Oral epithelial IL-22/STAT3 signaling licenses IL-17-mediated immunity to oral mucosal candidiasis
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IL-22 signaling limits oral candidiasis via proliferation of basal epithelial cells and replenishment of an IL-17–responsive layer.
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IL-22 appears dispensable for immunity in the setting of skin C. auris colonization, although it is critical for protection against C. albicans oral infection.
“The type-17 cytokine, IL-22, although critical for protection against C. albicans oral infection, appears dispensable for immunity in the setting of skin C. auris colonization [3,94].”
From Host–Candida auris interactions in the skin (2026) · cites this paper as [94]
The Results section reports that IL-22-deficient mice remained susceptible to oral C. albicans infection while wild-type mice cleared it, supporting the oral-protection part of the sentence. The paper does not address whether IL-22 is dispensable during skin C. auris colonization; its discussion of skin candidiasis concerns C. albicans, not C. auris. (LLM, conf=0.88)
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Cites
HISAT: a fast spliced aligner with low memory requirements
Kim, D., Langmead, B., & Salzberg, S. L. (2015) · Nature Methods · doi:10.1038/nmeth.3317 · Cited by 24,112 · see citing works
Differential expression analysis for sequence count data
Anders, S., & Huber, W. (2010) · Genome Biology · doi:10.1186/gb-2010-11-10-r106 · Cited by 15,581 · cited 1× · see citing works
“HISAT alignment files were used to generate read counts for each gene, and determination of differential gene expression was performed using the DE-seq package from Bioconductor (112).”
MethodHidden Killers: Human Fungal Infections
Brown, G. D., Denning, D. W., Gow, N. A. R., Levitz, S. M., Netea, M. G., & White, T. C. (2012) · Science Translational Medicine · doi:10.1126/scitranslmed.3004404 · Cited by 4,284 · see citing works
Surface phenotype and antigenic specificity of human interleukin 17–producing T helper memory cells
Acosta-Rodriguez, E. V., Rivino, L., Geginat, J., Jarrossay, D., Gattorno, M., Lanzavecchia, A., Sallusto, F., & Napolitani, G. (2007) · Nature Immunology · doi:10.1038/ni1467 · Cited by 1,828 · cited 1× · see citing works
“Moreover, C. albicans-specific Th17 cells recognize and provide cross-reactive protection against other fungal species, which is likely why maintaining C. albicans as a commensal is evolutionarily advantageous (78–81).”
BackgroundThe aryl hydrocarbon receptor links TH17-cell-mediated autoimmunity to environmental toxins
Veldhoen, M., Hirota, K., Westendorf, A. M., Buer, J., Dumoutier, L., Renauld, J.-C., & Stockinger, B. (2008) · Nature · doi:10.1038/nature06881 · Cited by 1,634 · see citing works
Hueber, W., Sands, B. E., Lewitzky, S., Vandemeulebroecke, M., Reinisch, W., Higgins, P. D. R., Wehkamp, J., Feagan, B. G., Yao, M. D., Karczewski, M., et al. (2012) · Gut · doi:10.1136/gutjnl-2011-301668 · Cited by 1,547 · cited 1× · see citing works
“In fact, IL-17 signaling in gut is generally more reparative than inflammatory (94–98), which is thought to explain why anti-IL-17 biologic therapies failed in treatment trials of Crohn’s disease (99).”
BackgroundFunctional Specialization of Interleukin-17 Family Members
Iwakura, Y., Ishigame, H., Saijo, S., & Nakae, S. (2011) · Immunity · doi:10.1016/j.immuni.2011.02.012 · Cited by 1,289 · see citing works
LeibundGut-Landmann, S., Groß, O., Robinson, M. J., Osorio, F., Slack, E. C., Tsoni, S. V., Schweighoffer, E., Tybulewicz, V., Brown, G. D., Ruland, J., et al. (2007) · Nature Immunology · doi:10.1038/ni1460 · Cited by 1,191 · see citing works
Fate mapping of IL-17-producing T cells in inflammatory responses
Hirota, K., Duarte, J. H., Veldhoen, M., Hornsby, E., Li, Y., Cua, D. J., Ahlfors, H., Wilhelm, C., Tolaini, M., Menzel, U., et al. (2011) · Nature Immunology · doi:10.1038/ni.1993 · Cited by 1,176 · cited 1× · see citing works
“This expression pattern contrasts to some extent with that of IL-17, based on prior studies using an IL-17A fate tracking reporter mouse (63) (Fig 2E) (29, 44).”
ResultIL-22 mediates mucosal host defense against Gram-negative bacterial pneumonia
Aujla, S. J., Chan, Y. R., Zheng, M., Fei, M., Askew, D. J., Pociask, D. A., Reinhart, T. A., McAllister, F. M., Edeal, J., Gaus, K., et al. (2008) · Nature Medicine · doi:10.1038/nm1710 · Cited by 1,162 · cited 1× · see citing works
“IL-17 and IL-22 are typically depicted signaling on the same cell types to mediate mucosal immunity, which is the case in non-stratified epithelia such as gut or lung (50, 84).”
BackgroundSelf-citationChronic Mucocutaneous Candidiasis in Humans with Inborn Errors of Interleukin-17 Immunity
Puel, A., Cypowyj, S., Bustamante, J., Wright, J. F., Liu, L., Lim, H. K., Migaud, M., Israel, L., Chrabieh, M., Audry, M., et al. (2011) · Science · doi:10.1126/science.1200439 · Cited by 1,056 · cited 2× · see citing works
“In humans, a family with IL-17F mutations has been described with CMC, suggesting a role in mucosal candidiasis (73).”
BackgroundConti, H. R., Shen, F., Nayyar, N., Stocum, E., Sun, J. N., Lindemann, M. J., Ho, A. W., Hai, J. H., Yu, J. J., Jung, J. W., et al. (2009) · Journal of Experimental Medicine · doi:10.1084/jem.20081463 · Cited by 1,024 · see citing works
Self-citationCandidalysin is a fungal peptide toxin critical for mucosal infection
Moyes, D. L., Wilson, D., Richardson, J. P., Mogavero, S., Tang, S. X., Wernecke, J., Hoefs, S., Gratacap, R. L., Robbins, J., Runglall, M., et al. (2016) · Nature · doi:10.1038/nature17625 · Cited by 928 · see citing works
Self-citationInterleukin-23-Independent IL-17 Production Regulates Intestinal Epithelial Permeability
Lee, J. S., Tato, C. M., Joyce-Shaikh, B., Gulen, M. F., Cayatte, C., Chen, Y., Blumenschein, W. M., Judo, M., Ayanoglu, G., McClanahan, T. K., et al. (2015) · Immunity · doi:10.1016/j.immuni.2015.09.003 · Cited by 760 · see citing works
Inflammatory memory sensitizes skin epithelial stem cells to tissue damage
Naik, S., Larsen, S. B., Gomez, N. C., Alaverdyan, K., Sendoel, A., Yuan, S., Polak, L., Kulukian, A., Chai, S., & Fuchs, E. (2017) · Nature · doi:10.1038/nature24271 · Cited by 745 · see citing works
Puel, A., Döffinger, R., Natividad, A., Chrabieh, M., Barcenas‐Morales, G., Pïcard, C., Cobat, A., Ouachée-Chardin, M., Toulon, A., Bustamante, J. C., et al. (2010) · The Journal of Experimental Medicine · doi:10.1084/jem.20091983 · Cited by 730 · cited 1× · see citing works
“In most mammals, though not mice, Th17 cells also express IL-26, a member of the same cytokine family as IL-22, and this cytokine may be also a target of biologic therapy (74); however, there is no evidence for autoantibodies against IL-26 in AIRE deficiency nor have IL-26-deficient humans been described (16).”
Vasioukhin, V., Degenstein, L., Wise, B., & Fuchs, E. (1999) · Proceedings of the National Academy of Sciences of the United States of America · doi:10.1073/pnas.96.15.8551 · Cited by 691 · cited 1× · see citing works
“To define the relative contributions of IL-22RA1 in oral epithelial cell subtypes, Il22ra1 fl/fl mice were crossed to K13 Cre or K14 CreERT2 mice (31, 65).”
MethodKisand, K. E., Wolff, A. S. B., Podkrajšek, K. T., Tserel, L., Link, M., Kisand, K., Ersvær, E., Perheentupa, J., Erichsen, M. M., Bratanič, N., et al. (2010) · The Journal of Experimental Medicine · doi:10.1084/jem.20091669 · Cited by 672 · see citing works
Qian, Y., Liu, C., Hartupee, J., Altuntas, C. Z., Gulen, M. F., Jane-wit, D., Xiao, J., Lu, Y., Giltiay, N., Liu, J., et al. (2007) · Nature Immunology · doi:10.1038/ni1439 · Cited by 614 · cited 1× · see citing works
“In fact, IL-17 signaling in gut is generally more reparative than inflammatory (94–98), which is thought to explain why anti-IL-17 biologic therapies failed in treatment trials of Crohn’s disease (99).”
BackgroundPlasticity of epithelial stem cells in tissue regeneration
Blanpain, C., & Fuchs, E. (2014) · Science · doi:10.1126/science.1242281 · Cited by 589 · see citing works
Wang, T., Fahrmann, J., Lee, H., Li, Y.-J., Tripathi, S. C., Yue, C., Zhang, C.-Y., Lifshitz, V., Song, J., Yuan, Y., et al. (2017) · Cell Metabolism · doi:10.1016/j.cmet.2017.11.001 · Cited by 580 · see citing works
IL‐23 and the Th17 pathway promote inflammation and impair antifungal immune resistance
Zelante, T., LUCA, A. D., Bonifazi, P., Montagnoli, C., Bozza, S., Moretti, S., Belladonna, M. L., Vacca, C., Conte, C., Mosci, P., et al. (2007) · European Journal of Immunology · doi:10.1002/eji.200737409 · Cited by 553 · see citing works
Sano, T., Huang, W., Hall, J. A., Yang, Y., Chen, A., Gavzy, S. J., Lee, J.-Y., Ziel, J. W., Miraldi, E. R., Domingos, A. I., et al. (2015) · Cell · doi:10.1016/j.cell.2015.08.061 · Cited by 547 · cited 4× · see citing works
“In some settings, IL-22 is induced in Th17 cells by the aryl hydrocarbon receptor (AhR) or serum amyloid A (SAA) (59, 60).”
BackgroundInfluentialCaspi, R., & Horai, R. (2011) · Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature · doi:10.3410/f.8304956.10813054 · Cited by 510 · see citing works
Human Anti-fungal Th17 Immunity and Pathology Rely on Cross-Reactivity against Candida albicans
Bacher, P., Hohnstein, T., Beerbaum, E., Röcker, M., Blango, M. G., Kaufmann, S., Röhmel, J., Eschenhagen, P., Grehn, C., Seidel, K., et al. (2019) · Cell · doi:10.1016/j.cell.2019.01.041 · Cited by 473 · see citing works
IL ‐22, not simply a Th17 cytokine
Rutz, S., Eidenschenk, C., & Ouyang, W. (2013) · Immunological Reviews · doi:10.1111/imr.12027 · Cited by 433 · see citing works
The adaptor protein CARD9 is required for innate immune responses to intracellular pathogens
Hsu, Y.-M. S., Zhang, Y., You, Y., Wang, D., Li, H., Duramad, O., Qin, F. X.-F., Dong, C., & Lin, X. (2006) · Nature Immunology · doi:10.1038/ni1426 · Cited by 420 · see citing works
Epithelial structural proteins of the skin and oral cavity: function in health and disease.
Presland, R., & Dale, B. (2000) · Critical Reviews in Oral Biology and Medicine · doi:10.1177/10454411000110040101 · Cited by 411 · cited 4× · see citing works
“Keratin 13 (K13) is expressed in differentiating SEL cells in the post-mitotic, terminally differentiated layer, which overlies the proliferative K14-expressing BEL (35).”
BackgroundInfluentialTissue-Specific Immunity at the Oral Mucosal Barrier
Moutsopoulos, N. M., & Konkel, J. E. (2017) · Trends in Immunology · doi:10.1016/j.it.2017.08.005 · Cited by 401 · see citing works
Wolk, K., Witte, E., Witte, K., Warszawska, K., & Sabat, R. (2010) · Seminars in Immunopathology · doi:10.1007/s00281-009-0188-x · Cited by 395 · see citing works
Dennehy, K. M., Ferwerda, G., Faro-Trindade, I., Pyż, E., Willment, J. A., Taylor, P. R., Kerrigan, A. M., Tsoni, S. V., Gordon, S., Meyer-Wentrup, F., et al. (2008) · European Journal of Immunology · doi:10.1002/eji.200737741 · Cited by 391 · see citing works
Gladiator, A., Wangler, N., Trautwein-Weidner, K., & LeibundGut-Landmann, S. (2013) · The Journal of Immunology · doi:10.4049/jimmunol.1202924 · Cited by 382 · cited 4× · see citing works
“Because mice are naïve to C. albicans, the IL-17 produced during a first encounter derives from innate immune cells (43–47).”
BackgroundResultInfluentialInterleukin-22 protects intestinal stem cells against genotoxic stress
Gronke, K., Hernández, P. P., Zimmermann, J., Klose, C. S. N., Kofoed-Branzk, M., Guendel, F., Witkowski, M., Tizian, C., Amann, L., Schumacher, F., et al. (2019) · Nature · doi:10.1038/s41586-019-0899-7 · Cited by 373 · cited 1× · see citing works
“IL-22RA1+ epithelial cells in colonic epithelium maintain genome integrity and limit apoptotic cell accumulation during genotoxic stress (91).”
BackgroundMAPK, MKP1 and c-Fos Discriminate Candida albicans Yeast from Hyphae in Epithelial Cells
Moyes, D., Runglall, M., Murciano, C., Shen, C., Nayar, D., Thavaraj, S., Kohli, A., Islam, A., Mora-Montes, H., Challacombe, S., et al. (2010) · Cell Host and Microbe · doi:10.1016/j.chom.2010.08.002 · Cited by 347 · see citing works
Self-citationGuttman-Yassky, E., Brunner, P. M., Neumann, A. U., Khattri, S., Pavel, A. B., Malik, K., Singer, G. K., Baum, D., Gilleaudeau, P., Sullivan-Whalen, M., et al. (2018) · Journal of the American Academy of Dermatology · doi:10.1016/j.jaad.2018.01.016 · Cited by 343 · cited 1× · see citing works
“Anti-IL-22 antibodies are under evaluation for skin pathologies such as atopic dermatitis (101), but rates of C. albicans infections have not been reported.”
BackgroundDifferential Roles for Interleukin-23 and Interleukin-17 in Intestinal Immunoregulation
Maxwell, J. R., Zhang, Y., Brown, W. A., Smith, C. L., Byrne, F. R., Fiorino, M., Stevens, E., Bigler, J., Davis, J. A., Rottman, J. B., et al. (2015) · Immunity · doi:10.1016/j.immuni.2015.08.019 · Cited by 342 · see citing works
Monin, L., & Gaffen, S. L. (2017) · Cold Spring Harbor Perspectives in Biology · doi:10.1101/cshperspect.a028522 · Cited by 338 · cited 1× · see citing works
“IL-17R signaling activity is generally restricted to non-hematopoietic cells (38, 39), and we previously demonstrated that IL-17RA in K13 + SEL cells is essential for immunity to OPC (31).”
BackgroundSelf-citationIL-17–Mediated Immunity to the Opportunistic Fungal Pathogen <i>Candida albicans</i>
Conti, H. R., & Gaffen, S. L. (2015) · The Journal of Immunology · doi:10.4049/jimmunol.1500909 · Cited by 301 · see citing works
Self-citationThe role of Dectin-1 in the host defence against fungal infections
Drummond, R. A., & Brown, G. D. (2011) · Current Opinion in Microbiology · doi:10.1016/j.mib.2011.07.001 · Cited by 294 · see citing works
IL-22 Is Required for Imiquimod-Induced Psoriasiform Skin Inflammation in Mice
Belle, A. V. V., de Heusch, M., Lemaire, M. M., Hendrickx, E., Warnier, G., Dunussi-joannopoulos, K., Fouser, L., Renauld, J., & Dumoutier, L. (2011) · Journal of Immunology · doi:10.4049/jimmunol.1102224 · Cited by 293 · see citing works
Pandiyan, P., Conti, H., Zheng, L.-X., Peterson, A. C., Mathern, D. R., Hernández-Santos, N., Edgerton, M., Gaffen, S., & Lenardo, M. (2011) · Immunity · doi:10.1016/j.immuni.2011.03.002 · Cited by 293 · see citing works
Self-citationSaunte, D. M., Mrowietz, U., Puig, L., & Zachariae, C. (2017) · British Journal of Dermatology · doi:10.1111/bjd.15015 · Cited by 280 · cited 1× · see citing works
“Anti-IL-17 biologics are associated with low but statistically significant rates of OPC, though it is rare for patients to stop therapy for this reason (100).”
BackgroundIL-22 defines a novel immune pathway of antifungal resistance
De Luca, A., Zelante, T., D'Angelo, C., Zagarella, S., Fallarino, F., Spreca, A., Iannitti, R. G., Bonifazi, P., Renauld, J.-C., Bistoni, F., et al. (2010) · Mucosal Immunology · doi:10.1038/mi.2010.22 · Cited by 265 · see citing works
Conti, H. R., Peterson, A. C., Brane, L., Huppler, A. R., Hernández-Santos, N., Whibley, N., Garg, A. V., Simpson-Abelson, M. R., Gibson, G. A., Mamo, A. J., et al. (2014) · Journal of Experimental Medicine · doi:10.1084/jem.20130877 · Cited by 254 · see citing works
Self-citationCandida albicans morphology and dendritic cell subsets determine T helper cell differentiation
Kashem, S. W., Igyártó, B. Z., Gerami-Nejad, M., Kumamoto, Y., Mohammed, J., Jarrett, E., Drummond, R. A., Zurawski, S. M., Zurawski, G., Berman, J., et al. (2015) · Immunity · doi:10.1016/j.immuni.2015.01.008 · Cited by 250 · see citing works
Self-citationGrowth Factor FGF2 Cooperates with Interleukin-17 to Repair Intestinal Epithelial Damage
Song, X., Dai, D., He, X., Zhu, S., Yao, Y., Gao, H., Wang, J., Qu, F., Qiu, J., Wang, H., et al. (2015) · Immunity · doi:10.1016/j.immuni.2015.06.024 · Cited by 244 · see citing works
Eyerich, K., Foerster, S., Rombold, S., Seidl, H., Behrendt, H., Hofmann, H., Ring, J., & Traidl‐Hoffmann, C. (2008) · Journal of Investigative Dermatology · doi:10.1038/jid.2008.139 · Cited by 241 · see citing works
IL-17 and IL-22: siblings, not twins
Eyerich, S., Eyerich, K., Cavani, A., & Schmidt‐Weber, C. B. (2010) · Trends in Immunology · doi:10.1016/j.it.2010.06.004 · Cited by 237 · cited 4× · see citing works
“In view of the many similar functions ascribed to IL-22 and IL-17 at mucosal surfaces (50), we asked whether IL-22 acts redundantly with IL-17 in OPC.”
BackgroundInfluentialCommensal Candida albicans Positively Calibrates Systemic Th17 Immunological Responses
Shao, T., Ang, W. X. G., Jiang, T. T., Huang, F. S., Andersen, H. M., Kinder, J. M., Pham, G. H., Burg, A. R., Ruff, B. P., Gonzalez, T., et al. (2019) · Cell Host & Microbe · doi:10.1016/j.chom.2019.02.004 · Cited by 237 · see citing works
Regulation of host-microbe interactions at oral mucosal barriers by type 17 immunity
Gaffen, S., & Moutsopoulos, N. (2020) · Science immunology · doi:10.1126/sciimmunol.aau4594 · Cited by 230 · see citing works
Self-citationKagami, S., Rizzo, H. L., Kurtz, S. E., Miller, L. S., & Blauvelt, A. (2010) · The Journal of Immunology · doi:10.4049/jimmunol.1001153 · Cited by 216 · see citing works
Adaptive immune responses to Candida albicans infection
Richardson, J. P., & Moyes, D. L. (2015) · Virulence · doi:10.1080/21505594.2015.1004977 · Cited by 206 · see citing works
Candidalysin: discovery and function in Candida albicans infections
Naglik, J., Gaffen, S., & Hube, B. (2019) · Current Opinion in Microbiology · doi:10.1016/j.mib.2019.06.002 · Cited by 203 · see citing works
Self-citationVerma, A. H., Richardson, J., Zhou, C., Coleman, B. M., Moyes, D., Ho, J., Huppler, A., Ramani, K., McGeachy, M., Mufazalov, I., et al. (2017) · Science immunology · doi:10.1126/sciimmunol.aam8834 · Cited by 203 · see citing works
Self-citationMouse model of oropharyngeal candidiasis
Solis, N. V., & Filler, S. G. (2012) · Nature Protocols · doi:10.1038/nprot.2012.011 · Cited by 195 · see citing works
Th17 cells confer long-term adaptive immunity to oral mucosal Candida albicans infections
Hernández‐Santos, N., Huppler, A. R., Peterson, A. C., Khader, S. A., McKenna, K. C., & Gaffen, S. L. (2012) · Mucosal Immunology · doi:10.1038/mi.2012.128 · Cited by 191 · see citing works
Self-citationPresland, R. B., & Jurevic, R. J. (2002) · Journal of Dental Education · doi:10.1002/j.0022-0337.2002.66.4.tb03536.x · Cited by 180 · cited 1× · see citing works
“The oral mucosa is among the most resilient epithelial surfaces (85).”
BackgroundZhu, W., Phan, Q. T., Boontheung, P., Solis, N. V., Loo, J. A., & Filler, S. G. (2012) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1117676109 · Cited by 180 · see citing works
Conti, H. R., Bruno, V. M., Childs, E. E., Daugherty, S., Hunter, J. P., Mengesha, B. G., Saevig, D. L., Hendricks, M. R., Coleman, B. M., Brane, L., et al. (2016) · Cell Host & Microbe · doi:10.1016/j.chom.2016.10.001 · Cited by 177 · see citing works
Self-citationCandidalysin activates innate epithelial immune responses via epidermal growth factor receptor
Ho, J., Yang, X., Nikou, S.-A., Kichik, N., Donkin, A., Ponde, N., Richardson, J., Gratacap, R. L., Archambault, L., Zwirner, C. P., et al. (2019) · Nature Communications · doi:10.1038/s41467-019-09915-2 · Cited by 176 · cited 5× · see citing works
“albicans from the mouth, although initially unexpected, is consistent with observations that AhR facilitates EGFR phosphorylation in OPC, a key step in fungal adhesion, endocytosis and invasion in OECs (25, 27, 82, 83).”
InfluentialSelf-citationDennehy, K. M., Willment, J. A., Williams, D. L., & Brown, G. D. (2009) · European Journal of Immunology · doi:10.1002/eji.200838543 · Cited by 176 · see citing works
Marks, B. R., Nowyhed, H. N., Choi, J.-Y., Poholek, A. C., Odegard, J., Flavell, R. A., & Craft, J. E. (2009) · Nature Immunology · doi:10.1038/ni.1783 · Cited by 173 · see citing works
EphA2 is an epithelial cell pattern recognition receptor for fungal β-glucans
Swidergall, M., Solis, N. V., Lionakis, M. S., & Filler, S. G. (2017) · Nature Microbiology · doi:10.1038/s41564-017-0059-5 · Cited by 167 · see citing works
Self-citationCandida albicans–epithelial interactions and induction of mucosal innate immunity
Naglik, J. R., König, A., Hube, B., & Gaffen, S. L. (2017) · Current Opinion in Microbiology · doi:10.1016/j.mib.2017.10.030 · Cited by 164 · cited 1× · see citing works
“albicans from a benign yeast morphotype to a damaging, invasive hyphal state (22).”
BackgroundSelf-citationLévy, R., Okada, S., Béziat, V., Moriya, K., Liu, C.-N., Chai, L., Migaud, M., Hauck, F., Ali, A. K. A., Cyrus, C., et al. (2016) · Proceedings of the National Academy of Sciences of the United States of America · doi:10.1073/pnas.1618300114 · Cited by 163 · cited 1× · see citing works
“While multiple families of CMC patients have been identified with mutations in IL-17R pathway genes (7, 72, 73), thus far no humans with genetic IL-22-deficiencies have been reported.”
BackgroundOkuma, A., Hoshino, K., Ohba, T., Fukushi, S., Aiba, S., Akira, S., Ono, M., Kaisho, T., & Muta, T. (2013) · Immunity · doi:10.1016/j.immuni.2012.11.016 · Cited by 157 · see citing works
New mechanism of oral immunity to mucosal candidiasis in hyper-IgE syndrome
Conti, H. R., Baker, O. J., Freeman, A. F., Jang, W. S., Holland, S. M., Li, R. A., Edgerton, M., & Gaffen, S. L. (2011) · Mucosal Immunology · doi:10.1038/mi.2011.5 · Cited by 132 · cited 1× · see citing works
“Supporting this, we found that HIES patients exhibit impairments in salivary antifungal immunity, with reduced levels of salivary AMPs including β-defensins and histatins (102).”
BackgroundSelf-citationYano, J., Lilly, E., Barousse, M., & Fidel, P. (2010) · Infection and Immunity · doi:10.1128/iai.00388-10 · Cited by 129 · see citing works
Candida-Host Interactions in HIV Disease
Fidel, P. L. (2011) · Advances in Dental Research · doi:10.1177/0022034511399284 · Cited by 128 · see citing works
Targeting STAT3 and oxidative phosphorylation in oncogene-addicted tumors
Lee, M., Hirpara, J. L., Eu, J. Q., Sethi, G., Wang, L., Goh, B.-C., & Wong, A. L. A. (2018) · Redox Biology · doi:10.1016/j.redox.2018.101073 · Cited by 128 · see citing works
Conti, H. R., Huppler, A. R., Whibley, N., & Gaffen, S. L. (2014) · Current Protocols in Immunology · doi:10.1002/0471142735.im1906s105 · Cited by 127 · cited 1× · see citing works
“To compare the roles of IL-22 and IL-17 in OPC, we tracked the time course of Il22 and Il17a mRNA expression in the oral mucosa (tongue) of wild-type (WT) immunocompetent mice following sublingual C. albicans infection (41, 42).”
BackgroundSelf-citationNew Model of Oropharyngeal Candidiasis in Mice
Kamai, Y., Kubota, M., Kamai, Y., Hosokawa, T., Fukuoka, T., & Filler, S. (2001) · Antimicrobial Agents and Chemotherapy · doi:10.1128/aac.45.11.3195-3197.2001 · Cited by 125 · see citing works
IL-17-mediated antifungal defense in the oral mucosa is independent of neutrophils
Trautwein-Weidner, K., Gladiator, A., Nur, S., Diethelm, P., & Leibundgut-Landmann, S. (2014) · Mucosal Immunology · doi:10.1038/mi.2014.57 · Cited by 116 · cited 1× · see citing works
“Interestingly, the capacity of IL-17 to drive oral neutrophil recruitment in OPC is not observed by all who use this OPC model (28, 75), possibly reflecting altered microbiota or other distinctions among animal facilities.”
BackgroundIL-1 Coordinates the Neutrophil Response to C. albicans in the Oral Mucosa
Altmeier, S., Toska, A., Sparber, F., Teijeira, A., Halin, C., & LeibundGut-Landmann, S. (2016) · PLOS Pathogens · doi:10.1371/journal.ppat.1005882 · Cited by 112 · cited 2× · see citing works
“Interestingly, the capacity of IL-17 to drive oral neutrophil recruitment in OPC is not observed by all who use this OPC model (28, 75), possibly reflecting altered microbiota or other distinctions among animal facilities.”
BackgroundEckhardt, E. R. M., Witta, J., Zhong, J., Arsenescu, R. I., Arsenescu, V., Wang, Y., Ghoshal, S., de Beer, M. C., de Beer, F. C., & de Villiers, W. J. S. (2010) · BMC Gastroenterology · doi:10.1186/1471-230x-10-133 · Cited by 109 · see citing works
Borghi, M., Luca, A. D., Puccetti, M., Jaeger, M., Mencacci, A., Oikonomou, V., Pariano, M., Garlanda, C., Moretti, S., Bartoli, A., et al. (2015) · Cell Host and Microbe · doi:10.1016/j.chom.2015.07.004 · Cited by 107 · cited 1× · see citing works
“In non-oral manifestations of C. albicans infection or colonization (systemic, vaginal, dermal or gastric), IL-22 is not necessarily protective, emphasizing that specific cytokine responses even to the same pathogen are influenced by tissue milieu (12, 40, 68–71).”
BackgroundGenini, D., Brambilla, L., Laurini, E., Merulla, J., Civenni, G., Pandit, S., D'Antuono, R., Perez, L., Levy, D. E., Pricl, S., et al. (2017) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1615730114 · Cited by 106 · cited 1× · see citing works
“STAT3 also regulates metabolism in various settings to meet energy needs for cell proliferation, and STAT3-regulated functions in mitochondria are becoming increasingly appreciated (104–106).”
BackgroundYano, J., Kolls, J., Happel, K., Wormley, F., Wozniak, K., & Fidel, P. (2012) · PLoS ONE · doi:10.1371/journal.pone.0046311 · Cited by 106 · see citing works
Self-citationA Novel Th Cell Epitope of Candida albicans Mediates Protection from Fungal Infection
Bär, E., Gladiator, A., Bastidas, S., Roschitzki, B., Acha-Orbea, H., Oxenius, A., & Leibundgut-Landmann, S. (2012) · Journal of Immunology · doi:10.4049/jimmunol.1200594 · Cited by 104 · cited 2× · see citing works
“Because mice are naïve to C. albicans, the IL-17 produced during a first encounter derives from innate immune cells (43–47).”
BackgroundInborn errors of immunity underlying fungal diseases in otherwise healthy individuals
Li, J., Vinh, D. C., Casanova, J., & Puel, A. (2017) · Current Opinion in Microbiology · doi:10.1016/j.mib.2017.10.016 · Cited by 103 · see citing works
Moyes, D., Shen, C.-G., Murciano, C., Runglall, M., Richardson, J., Arno, M., Aldecoa-Otalora, E., & Naglik, J. (2013) · Journal of Infectious Diseases · doi:10.1093/infdis/jit824 · Cited by 102 · see citing works
Self-citationInnate Defense against Fungal PathogensPreprint
Drummond, R. A., Gaffen, S. L., Hise, A. G., & Brown, G. D. (2014) · Cold Spring Harbor Perspectives in Medicine · doi:10.1101/cshperspect.a019620 · Cited by 102 · see citing works
Self-citationOropharyngeal Candidiasis: Fungal Invasion and Epithelial Cell Responses
Swidergall, M., & Filler, S. (2017) · PLoS Pathogens · doi:10.1371/journal.ppat.1006056 · Cited by 101 · cited 1× · see citing works
“The finding that AhR was not essential to induce IL-22 or clear C. albicans from the mouth, although initially unexpected, is consistent with observations that AhR facilitates EGFR phosphorylation in OPC, a key step in fungal adhesion, endocytosis and invasion in OECs (25, 27, 82, 83).”
ResultThe cup runneth over: lessons from the ever-expanding pool of primary immunodeficiency diseases
Milner, J. D., & Holland, S. M. (2013) · Nature reviews. Immunology · doi:10.1038/nri3493 · Cited by 98 · cited 3× · see citing works
“AIRE-deficient humans have circulating neutralizing Abs against IL-17F, IL-22 and IL-17A, thought to help explain the CMC manifestations in these patients (9, 16–18).”
BackgroundInfluentialWu, W., Hsu, Y.-M. S., Bi, L.-K., Zhou, S.-Y., & Lin, X. (2009) · Nature Immunology · doi:10.1038/ni.1788 · Cited by 96 · cited 1× · see citing works
“Conventional adaptive Th17 responses to C. albicans are triggered by sensing of β -glucans in the fungal cell wall via the Dectin-1/CARD9 signaling, which induces Th17-polarizing cytokines (IL-23 and IL-6) (52–58).”
BackgroundDevelopment of vaccines for Candida albicans: fighting a skilled transformer
Cassone, A. (2013) · Nature Reviews Microbiology · doi:10.1038/nrmicro3156 · Cited by 93 · see citing works
β-Defensin 1 Plays a Role in Acute Mucosal Defense against Candida albicans
Tomalka, J. A., Azodi, E., Narra, H. P., Patel, K., O’Neill, S., Cardwell, C., Hall, B. A., Wilson, J. M., & Hise, A. G. (2015) · The Journal of Immunology · doi:10.4049/jimmunol.1203239 · Cited by 92 · see citing works
IL-36 and IL-1/IL-17 drive immunity to oral candidiasis via parallel mechanisms
Verma, A. H., Zafar, H. M., Ponde, N., Hepworth, O. W., Sihra, D., Aggor, F. E. Y., Ainscough, J. S., Ho, J., Richardson, J., Coleman, B. M., et al. (2018) · Journal of Immunology · doi:10.4049/jimmunol.1800515 · Cited by 91 · see citing works
Self-citationAutoimmune Polyendocrine Syndromes: Clues to Type 1 Diabetes Pathogenesis
Husebye, E. S., & Anderson, M. S. (2010) · Immunity · doi:10.1016/j.immuni.2010.03.016 · Cited by 85 · cited 1× · see citing works
“For example, OPC occurs in patients with autoimmune polyendocrine syndrome type 1 (APS-1), a congenital autoimmune syndrome caused by mutations in AIRE and characterized by circulating auto-antibodies that neutralize not only IL-17A and IL-17F but also IL-22 (16–19).”
BackgroundFarah, C., Hu, Y., Riminton, S., & Ashman, R. (2006) · Oral Microbiology and Immunology · doi:10.1111/j.1399-302x.2006.00288.x · Cited by 82 · see citing works
Interleukin-17-induced protein lipocalin 2 is dispensable for immunity to oral candidiasis
Ferreira, M. C., Whibley, N., Mamo, A. J., Siebenlist, U., Chan, Y. R., & Gaffen, S. L. (2014) · Infection and Immunity · doi:10.1128/iai.01389-13 · Cited by 72 · see citing works
Self-citationClancy, C., Cheng, S.-J., & Nguyen, M. H. (2009) · Methods in molecular biology · doi:10.1007/978-1-60327-151-6_8 · Cited by 71 · see citing works
Innate Immunity to Mucosal Candida Infections
Verma, A. H., Gaffen, S. L., & Swidergall, M. (2017) · Journal of Fungi · doi:10.3390/jof3040060 · Cited by 66 · cited 1× · see citing works
“Hyphal invasion thus establishes an inflammatory milieu that is initiated by candidalysin-induced SEL damage, potentiated by IL-17- and candidalysin-induced effectors such as IL-1 and IL-36, and ultimately resolved upon clearance of the pathogen (29, 88).”
BackgroundSelf-citationLineage Analysis of Epidermal Stem CellsPreprint
Alcolea, M. P., & Jones, P. H. (2014) · Cold Spring Harbor Perspectives in Medicine · doi:10.1101/cshperspect.a015206 · Cited by 65 · see citing works
Gut-busters -- IL-17 Ain’t Afraid Of No IL-23
Whibley, N., & Gaffen, S. (2015) · Immunity · doi:10.1016/j.immuni.2015.10.001 · Cited by 65 · cited 1× · see citing works
“In fact, IL-17 signaling in gut is generally more reparative than inflammatory (94–98), which is thought to explain why anti-IL-17 biologic therapies failed in treatment trials of Crohn’s disease (99).”
BackgroundSelf-citationAntibody blockade of IL-17 family cytokines in immunity to acute murine oral mucosal candidiasis
Whibley, N., Tritto, E., Traggiai, E., Kolbinger, F., Moulin, P., Brees, D., Coleman, B. M., Mamo, A. J., Garg, A. V., Jaycox, J. R., et al. (2016) · Journal of Leukocyte Biology · doi:10.1189/jlb.4a0915-428r · Cited by 65 · see citing works
Self-citationTrautwein-Weidner, K., Gladiator, A., Kirchner, F. R., Becattini, S., Rülicke, T., Sallusto, F., & LeibundGut‐Landmann, S. (2015) · PLoS Pathogens · doi:10.1371/journal.ppat.1005164 · Cited by 64 · see citing works
Chronic mucocutaneous candidiasis and congenital susceptibility to Candida
Glocker, E. O., & Grimbacher, B. (2010) · Current Opinion in Allergy and Clinical Immunology · doi:10.1097/aci.0b013e32833fd74f · Cited by 63 · see citing works
Bishu, S., Hernández‐Santos, N., Simpson-Abelson, M. R., Huppler, A. R., Conti, H. R., Ghilardi, N., Mamo, A. J., & Gaffen, S. L. (2013) · Infection and Immunity · doi:10.1128/iai.01335-13 · Cited by 63 · see citing works
Self-citationThe Aryl Hydrocarbon Receptor Governs Epithelial Cell Invasion during Oropharyngeal Candidiasis
Solis, N., Swidergall, M., Bruno, V. M., Gaffen, S., & Filler, S. (2017) · mBio · doi:10.1128/mbio.00025-17 · Cited by 61 · see citing works
Self-citationSparber, F., Dolowschiak, T., Mertens, S., Lauener, L., Clausen, B., Joller, N., Stoitzner, P., Tussiwand, R., & Leibundgut-Landmann, S. (2018) · PLoS Pathogens · doi:10.1371/journal.ppat.1007069 · Cited by 52 · see citing works
Critical role of IL22/IL22RA1 signaling in pneumococcal pneumonia
Trevejo-Nuñez, G., Elsegeiny, W., Conboy, P., Chen, K., & Kolls, J. (2016) · Journal of Immunology · doi:10.4049/jimmunol.1600528 · Cited by 52 · see citing works
Self-citationInterleukin-26: An Emerging Player in Host Defense and Inflammation
Tengvall, S., Che, K., & Lindén, A. (2015) · Journal of Innate Immunity · doi:10.1159/000434646 · Cited by 50 · cited 1×
“…though not mice, Th17 cells also express IL-26, a member of the same cytokine family as IL-22, and this cytokine may be also a target of biologic therapy (74); however, there is no evidence for autoantibodies against IL-26 in AIRE deficiency nor have IL-26-deficient humans been described (16).”
BackgroundPeters, B. M., Coleman, B. M., Willems, H. M. E., Barker, K. S., Aggor, F. E. Y., Cipolla, E., Verma, A. H., Bishu, S., Huppler, A. R., Bruno, V. M., et al. (2019) · The Journal of Infectious Diseases · doi:10.1093/infdis/jiz649 · Cited by 44 · see citing works
Self-citationZelante, T., Iannitti, R. G., LUCA, A. D., & Romani, L. R. (2011) · European Journal of Immunology · doi:10.1002/eji.201041246 · Cited by 42 · see citing works
Shen, F., Verma, A. H., Volk, A. L., Jones, B. H., Coleman, B. M., Loza, M. J., Malaviya, R., Moore, B. A., Weinstock, D., Elloso, M. M., et al. (2019) · The Journal of Immunology · doi:10.4049/jimmunol.1801436 · Cited by 29 · see citing works
Self-citationNeutrophils Do Not Express IL-17A in the Context of Acute Oropharyngeal Candidiasis
Huppler, A. R., Verma, A. H., Conti, H. R., & Gaffen, S. L. (2015) · Pathogens · doi:10.3390/pathogens4030559 · Cited by 26 · cited 1× · see citing works
“We previously showed that antigen-independent CD4+TCRαβ+ cells that express IL-17 [‘natural’ Th17 cells, nTh17 (48)] are required for effective immunity to OPC (29, 44, 49).”
BackgroundSelf-citationIL-22 neutralizing autoantibodies impair fungal clearance in murine oropharyngeal candidiasis model
Bichele, R., Kärner, J., Truusalu, K., Smidt, I., Mändar, R., Conti, H., Gaffen, S., Peterson, P., Laan, M., & Kisand, K. (2017) · European Journal of Immunology · doi:10.1002/eji.201747209 · Cited by 26 · cited 1× · see citing works
“Mice with IL-22 impairments (via gene deficiency or antibody neutralization) are susceptible to OPC (12, 20, 21), and reduced IL-22 expression is associated with human chronic mucocutaneous candidiasis (CMC) (8).”
BackgroundSelf-citationGoupil, M., Cousineau-Côté, V., Aumont, F., Sénéchal, S., Gaboury, L., Hanna, Z., Jolicoeur, P., & de Repentigny, L. (2014) · BMC Immunology · doi:10.1186/s12865-014-0049-9 · Cited by 23 · cited 1× · see citing works
“Mice with IL-22 impairments (via gene deficiency or antibody neutralization) are susceptible to OPC (12, 20, 21), and reduced IL-22 expression is associated with human chronic mucocutaneous candidiasis (CMC) (8).”
BackgroundIsolation of T cells from mouse oral tissues
Pandiyan, P., Bhaskaran, N., Zhang, Y., & Weinberg, A. (2014) · Biological Procedures Online · doi:10.1186/1480-9222-16-4 · Cited by 22 · see citing works
IL-22-Expressing Murine Lymphocytes Display Plasticity and Pathogenicity in Reporter Mice
Shen, W., Hixon, J. A., McLean, M. H., Li, W., & Durum, S. K. (2016) · Frontiers in Immunology · doi:10.3389/fimmu.2015.00662 · Cited by 21 · cited 2× · see citing works
“IL-22 protein levels were similarly affected, assessed using IL22TdTomato reporter mice (62) (fig.”
Self-citationAnti‐cytokine autoantibodies explain some chronic mucocutaneous candidiasis
Browne, S., & Holland, S. M. (2010) · Immunology and Cell Biology · doi:10.1038/icb.2010.72 · Cited by 19 · see citing works
d’Enfert, C., & Bougnoux, M. (2014) · Elsevier eBooks · doi:10.1016/b978-0-12-801238-3.00139-2 · Cited by 15 · cited 1× · see citing works
“INTRODUCTION Fungal infections are a serious threat to public health, but our understanding of immunity to fungi lags behind that of other microbes (1).”
BackgroundFungus Among Us: The Frenemies Within
Aggor, F. E. Y., Way, S. S., & Gaffen, S. L. (2019) · Trends in Immunology · doi:10.1016/j.it.2019.04.007 · Cited by 3 · see citing works
Self-citation
Flagged first, then by citations
8 of the 123 references couldn’t be matched to a known paper.
Research works printed but not linked: 4
- [13]Ho A, IL-17RC is required for immune signaling via an extended SEF/IL-17R signaling domain in the cytoplasmic tail. J. Immunol 185, 1063– 1070 (2010). 20554964 PMC2897912
- [23]Moyes DL, A biphasic innate immune MAPK response discriminates between the yeast and hyphal forms of Candida albicans in epithelial cells. Cell Host Microbe 8, 225– 235 (2010). 20833374 PMC2991069
- [31]Conti H, IL-17RA signaling in oral epithelium is critical for protection against oropharyngeal candidiasis. Cell Host Microbe 20, 606– 617 (2016). 27923704 PMC5147498
- [64]Wolk K, Witte E, Witte K, Warszawska K, Sabat R, Biology of IL-22. Semin Immunol 32, 17– 31 (2010). 20127093
Cited by
Sorted by citations
Pathogenesis and virulence of Candida albicans
Lopes, J. P., & Lionakis, M. S. (2021) · Virulence · doi:10.1080/21505594.2021.2019950 · Cited by 511 · see citing works
“IL-22 is another cytokine produced by type 17 innate and adaptive lymphoid cell subsets during OPC and plays an important role in antifungal resistance as shown by experiments in Il22r−/− mice, in wild-type mice administered IL-22-targeted mAbs, and in mice deficient in both IL-17R and IL-22R, which exhibit further in…”
BackgroundSelf-citationImmunological mechanisms of inflammatory diseases caused by gut microbiota dysbiosis: A review
Zhao, M., Chu, J., Feng, S., Guo, C., Xue, B., He, K., & Li, L. (2023) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2023.114985 · Cited by 466 · see citing works
Immune responses to human fungal pathogens and therapeutic prospects
Lionakis, M. S., Drummond, R. A., & Hohl, T. M. (2023) · Nature Reviews Immunology · doi:10.1038/s41577-022-00826-w · Cited by 379 · see citing works
Self-citationA pan-cancer mycobiome analysis reveals fungal involvement in gastrointestinal and lung tumors
Dohlman, A. B., Klug, J., Mesko, M., Gao, I. H., Lipkin, S. M., Shen, X., & Iliev, I. D. (2022) · Cell · doi:10.1016/j.cell.2022.09.015 · Cited by 420 · see citing works
d’Enfert, C., Kaune, A.-K., Alaban, L. R., Chakraborty, S., Cole, N. L., Delavy, M., Kosmala, D., Marsaux, B., Fróis-Martins, R., Morelli, M., et al. (2020) · FEMS Microbiology Reviews · doi:10.1093/femsre/fuaa060 · Cited by 351 · see citing works
Mucosal fungi promote gut barrier function and social behavior via Type 17 immunity
Leonardi, I., Gao, I. H., Lin, W.-Y., Allen, M., Li, X. V., Fiers, W. D., De Celie, M. B., Putzel, G. G., Yantiss, R. K., Johncilla, M., et al. (2022) · Cell · doi:10.1016/j.cell.2022.01.017 · Cited by 307 · see citing works
Lin, D., Yang, L. Y., Wen, L., Lu, H., Chen, Q., & Wang, Z. (2021) · Mucosal Immunology · doi:10.1038/s41385-021-00413-7 · Cited by 190 · see citing works
“albicans transition from a benign yeast morphotype to a damaging, invasive hyphal state.(29) This early recognition is partially mediated by epidermal growth factor receptor (EGFR) family receptors and involves sensing the oral tissue damage induced by candidalysin.”
BackgroundAberrant type 1 immunity drives susceptibility to mucosal fungal infections.
Break, T. J., Oikonomou, V., Dutzan, N., Desai, J. V., Swidergall, M., Freiwald, T., Chauss, D., Harrison, O. J., Alejo, J., Williams, D. W., et al. (2021) · Science · doi:10.1126/science.aay5731 · Cited by 175 · see citing works
“Neutrophils have been reported to promote normal fungal clearance in the oralmucosa,where they accumulate in an IL-17R– and IL-22–dependent manner during OPC (24, 25).”
BackgroundMethodInfluentialSelf-citationDrummond, R. A., Desai, J. V., Ricotta, E. E., Swamydas, M., Deming, C., Conlan, S., Quinones, M., Matei-Rascu, V., Sheriff, L., Lecky, D., et al. (2022) · Cell Host & Microbe · doi:10.1016/j.chom.2022.04.013 · Cited by 141 · see citing works
Self-citationCommensalism and pathogenesis of Candida albicans at the mucosal interface
Schille, T. B., Sprague, J. L., Naglik, J. R., Brunke, S., & Hube, B. (2025) · Nature Reviews Microbiology · doi:10.1038/s41579-025-01174-x · Cited by 77 · see citing works
“148–150).”
Self-citationApplications of Plasma-Activated Water in Dentistry: A Review
Milhan, N., Chiappim, W., Sampaio, A. D. G., Vegian, M. R. D. C., Pessoa, R., & Koga-Ito, C. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23084131 · Cited by 70 · see citing works
McCrory, C., Lenardon, M. D., & Traven, A. (2024) · Trends in Microbiology · doi:10.1016/j.tim.2024.04.004 · Cited by 68 · see citing works
The Interactions Between Candida albicans and Mucosal Immunity
Zhou, Y., Cheng, L., Lei, Y. L., Ren, B., & Zhou, X. (2021) · Frontiers in Microbiology · doi:10.3389/fmicb.2021.652725 · Cited by 65 · see citing works
“essential in the oral basal epithelial layer and can cooperate with IL-17 signaling in the oral mucosa (Aggor et al., 2020).”
BackgroundCandida albicans and candidalysin in inflammatory disorders and cancer
Ho, J., Camilli, G., Griffiths, J. S., Richardson, J., Kichik, N., & Naglik, J. (2020) · Immunology · doi:10.1111/imm.13255 · Cited by 62 · see citing works
Self-citationWestman, J., Plumb, J. D., Licht, A., Yang, M., Allert, S., Naglik, J. R., Hube, B., Grinstein, S., & Maxson, M. E. (2022) · Cell Reports · doi:10.1016/j.celrep.2021.110187 · Cited by 58 · see citing works
“We also tested the effects of IL-22, which was reported to protect epithelia during oral candidiasis in vivo (Conti et al., 2009; Bichele et al., 2018; Aggor et al., 2020).”
BackgroundSelf-citationWu, Y., Du, S., Bimler, L., Mauk, K. E., Lortal, L., Kichik, N., Griffiths, J. S., Osicka, R., Song, L.-Z., Polsky, K., et al. (2023) · Cell Reports · doi:10.1016/j.celrep.2023.113240 · Cited by 52 · see citing works
Self-citationCandidalysin triggers epithelial cellular stresses that induce necrotic death
Blagojevic, M., Camilli, G., Maxson, M. E., Hube, B., Moyes, D., Richardson, J., & Naglik, J. (2021) · Cellular Microbiology · doi:10.1111/cmi.13371 · Cited by 52 · see citing works
“…candidalysin (encoded by the ECE1 gene) is a key driver of cell damage and immune responses in mucosal and systemic models of C. albicans infection (Aggor et al., 2020; Allert et al., 2018; Drummond et al., 2019; Ho et al., 2019; Ho et al., 2020; Kasper et al., 2018; Moyes et al., 2016; Richardson…”
BackgroundSelf-citationInflammatory and Immunological Basis of Periodontal Diseases
Baima, G., Arce, M., Romandini, M., & Dyke, T. E. V. (2025) · Journal of Periodontal Research · doi:10.1111/jre.70040 · Cited by 49 · see citing works
Role of the microbiome in oral cancer occurrence, progression and therapy
Li, Z., Liu, Y., & Zhang, L. (2022) · Microbial Pathogenesis · doi:10.1016/j.micpath.2022.105638 · Cited by 48 · see citing works
Breakdown of Symbiosis in Radiation-Induced Oral Mucositis
Ingrosso, G., Saldi, S., Marani, S., Wong, A. Y., Bertelli, M., Aristei, C., & Zelante, T. (2021) · Journal of Fungi · doi:10.3390/jof7040290 · Cited by 45 · see citing works
“[37] demonstrated that, during oral Candida infection in a murine experimental model, basal epithelial cells expressed high levels of IL-22 receptor (R), which binds IL-22 also released by Th17 cells.”
BackgroundIs Candida albicans a contributor to cancer? A critical review based on the current evidence
Wang, X., Zhang, W., Wu, W., Wu, S., Young, A., & Yan, Z. (2023) · Microbiological Research · doi:10.1016/j.micres.2023.127370 · Cited by 44 · see citing works
Laska, J., Tota, M., Łacwik, J., Sędek, Ł., & Gomułka, K. (2024) · Cells · doi:10.3390/cells13161398 · Cited by 51 · see citing works
“Studies have shown that, compared to placebo, it significantly improves the clinical signs and symptoms of AD, is well tolerated, and shifts the lesion transcriptome toward a lesion‑free phenotype [116].”
BackgroundResultMicrobiota-mediated mechanisms of mucosal immunity across the lifespan
Iliev, I. D., Blander, J. M., Collins, N., Guo, C., Longman, R., Sonnenberg, G. F., Zeng, M. Y., & Artis, D. (2025) · Nature Immunology · doi:10.1038/s41590-025-02281-w · Cited by 43 · see citing works
“IL-22 activates regenerative signals on oral epithelial cells through IL-22RA and IL-10RB to foster the proliferation and repair of IL-17R-expressing epithelial cells that respond to IL-17 and mediate antifungal events 171 .”
The interplay between oral microbes and immune responses
Liu, Y., Qv, W., Ma, Y., Zhang, Y., Ding, C., Chu, M., & Chen, F. (2022) · Frontiers in Microbiology · doi:10.3389/fmicb.2022.1009018 · Cited by 40 · see citing works
“These effectors promote a neutrophil response and direct fungicidal activity to maintain barrier integrity (Aggor et al., 2020).”
BackgroundInflammatory cytokine signalling in vulvovaginal candidiasis: a hot mess driving immunopathology
Cheng, K. O., Montaño, D. E., Zelante, T., Dietschmann, A., & Gresnigt, M. S. (2024) · Oxford Open Immunology · doi:10.1093/oxfimm/iqae010 · Cited by 38 · see citing works
“…have been associated with crucial roles in mediating neutrophil recruitment, production of antimicrobial peptides (AMPs) and epithelial regeneration [148–150], yet the importance and roles of these responses during VVC are difficult to interpret due to the variability in results between studies.”
BackgroundT cell responses to control fungal infection in an immunological memory lens
Sharma, J., Mudalagiriyappa, S., & Nanjappa, S. G. (2022) · Frontiers in Immunology · doi:10.3389/fimmu.2022.905867 · Cited by 38 · see citing works
Cutaneous and subcutaneous fungal infections: recent developments on host–fungus interactions
Ma, Y., Wang, X., & Li, R. (2021) · Current Opinion in Microbiology · doi:10.1016/j.mib.2021.05.005 · Cited by 35 · see citing works
New insights into immunity to skin fungi shape our understanding of health and disease
Ruchti, F., & LeibundGut‐Landmann, S. (2023) · Parasite Immunology · doi:10.1111/pim.12948 · Cited by 31 · see citing works
“IL-17 receptor expression was proposed to be enhanced by IL-22 in a model of oral candidiasis.(63) Beyond CD4 T cells, other lymphoid cells contribute to the overall IL-17 response to commensal fungi including CD8 T cells, dermal γδ T cells and TCR-negative innate lymphoid cells (ILCs).”
BackgroundTissue Damage in Radiation-Induced Oral Mucositis Is Mitigated by IL-17 Receptor Signaling
Saul-Mcbeth, J., Dillon, J., Lee, A., Launder, D., Kratch, J. M., Abutaha, E., Williamson, A., Schroering, A. G., Michalski, G., Biswas, P., et al. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.687627 · Cited by 30 · see citing works
“cavity require healing and restoration of the epithelium, but the injury is not as easily followed to the healing phase (54).”
BackgroundSelf-citationIncreased STAT3 Activation in Periodontitis Drives Inflammatory Bone Loss
Arce, M., Rodríguez-Peña, M., Espinoza-Arrue, J., Godoy, R. A., Reyes, M., Kajikawa, T., Greenwell-Wild, T., Hajishengallis, G., Abusleme, L., Moutsopoulos, N., et al. (2023) · Journal of dentistry research · doi:10.1177/00220345231192381 · Cited by 28 · see citing works
“In the oral mucosa, STAT3 activation has been associated with wound-healing processes and immunity to Candida albicans , underscoring its importance in the oral epithelium homeostasis (Yu et al. 2016; Aggor et al. 2020).”
BackgroundLi, H., Wang, Y.-Q., Duan, H.-X., Bao, Y., Deng, X., He, Y., Gao, Q., Li, P.-J., & Liu, X.-D. (2025) · Frontiers in Immunology · doi:10.3389/fimmu.2025.1651808 · Cited by 27 · see citing works
“Critically, IL-22 and IL-17 form a synergistic axis: IL-22 de fi ciency ampli fi es IL-17-driven in fl ammation, whereas IL-22 supplementation restores bacterial clearance and attenuates in fl ammation (167) ―”
Russell, C. M., Rybak, J. A., Miao, J., Peters, B. M., & Barrera, F. N. (2022) · Journal of Biological Chemistry · doi:10.1016/j.jbc.2022.102829 · Cited by 26 · see citing works
“IL22 is another major effector of the IL-17 signaling axis, and its expression is similarly reduced in oral epithelium during challenge with an ece1Δ/Δ or CL deletion strain as compared to infection with the WT strain (43).”
BackgroundThe evil companion of OSCC : Candida albicans
Yang, Z., Zhang, S., Ji, N., Li, J., & Chen, Q. (2023) · Oral Diseases · doi:10.1111/odi.14700 · Cited by 23 · see citing works
Vaccine protection by Cryptococcus neoformans Δsgl1 is mediated by γδ T cells via TLR2 signaling
Normile, T. G., Chu, T. H., Sheridan, B., & Poeta, M. D. (2022) · Mucosal Immunology · doi:10.1038/s41385-022-00570-3 · Cited by 23 · see citing works
“Although IL-17 has been implicated as a potent antifungal effector cytokine in other fungal infections 72–76 , the requirement for IL-17 in host defense against C. neoformans remains uncertain 77–80 .”
IκBζ is an essential mediator of immunity to oropharyngeal candidiasis
Taylor, T. C., Coleman, B. M., Arunkumar, S. P., Dey, I., Dillon, J. T., Ponde, N. O., Poholek, A. C., Schwartz, D. M., McGeachy, M. J., Conti, H. R., et al. (2023) · Cell Host & Microbe · doi:10.1016/j.chom.2023.08.016 · Cited by 25 · see citing works
Self-citationA gut-oral microbiome–driven axis controls oropharyngeal candidiasis through retinoic acid
Aggor, F. E. Y., Bertolini, M., Zhou, C., Taylor, T. C., Abbott, D. A., Musgrove, J., Bruno, V. M., Hand, T. W., & Gaffen, S. L. (2022) · JCI Insight · doi:10.1172/jci.insight.160348 · Cited by 20 · see citing works
“Mielke LA, et al. Retinoic acid expression associates with enhanced IL-22 production by γδ T cells and innate lymphoid cells and attenuation of intestinal inflammation.”
BackgroundResultInfluentialSelf-citationBorgström, E. W., Edvinsson, M., Pérez, L., Norlin, A., Enoksson, S. L., Hansen, S., Fasth, A., Friman, V., Kämpe, O., Månsson, R., et al. (2022) · Journal of Clinical Immunology · doi:10.1007/s10875-022-01351-0 · Cited by 21 · see citing works
“17A, IL-17F [15], and IL-22 which are important cytokines for mucosal immunity [16].”
BackgroundCombinatorial actions of IL-22 and IL-17 drive optimal immunity to oral candidiasis through SPRRs
Aggor, F. E. Y., Bertolini, M., Coleman, B. M., Taylor, T. C., Ponde, N. O., & Gaffen, S. (2024) · PLoS Pathogens · doi:10.1371/journal.ppat.1012302 · Cited by 20 · see citing works
Self-citationCandida albicans Virulence Traits in Commensalism and Disease
Fróis-Martins, R., Lagler, J., & LeibundGut‐Landmann, S. (2024) · Current Clinical Microbiology Reports · doi:10.1007/s40588-024-00235-8 · Cited by 19 · see citing works
“IL-17 and IL-22 cytokines prevent excessive fungal growth on the epithelia, presumably via the induction of antimicrobial peptides in epithelial cells [18–20].”
Yamanaka-Takaichi, M., Ghanian, S., Katzka, D., Torgerson, R., & Alavi, A. (2022) · American Journal of Clinical Dermatology · doi:10.1007/s40257-022-00686-z · Cited by 19 · see citing works
Neonatal T Helper 17 Responses Are Skewed Towards an Immunoregulatory Interleukin-22 Phenotype
Razzaghian, H., Sharafian, Z., Sharma, A. A., Boyce, G. K., Lee, K., Silva, R. D., Orban, P., Sékaly, R., Ross, C., & Lavoie, P. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.655027 · Cited by 17 · see citing works
“the gut), such as gd T cells or type 3 innate lymphoid cells (31, 51), or other T cell subsets in peripheral tissues (52).”
BackgroundAct Locally, Act Globally—Microbiota, Barriers, and Cytokines in Atherosclerosis
Kurilenko, N., Fatkhullina, A. R., Mazitova, A., & Koltsova, E. K. (2021) · Cells · doi:10.3390/cells10020348 · Cited by 22 · see citing works
Pasman, R., Krom, B. P., Zaat, S. A. J., & Brul, S. (2022) · Frontiers in Oral Health · doi:10.3389/froh.2022.851786 · Cited by 16 · see citing works
“Additional to AMP induction, PAMPs of C. albicans hyphae and produced candidalysin activate the epidermal growth factor receptor (EGFR) and ephrin type-A receptor 2 (EphA2) of oral ECs and, thereby, induce the release of pro-inflammatory cytokines and chemokines which attract neutrophils to the site of infection [37, 3…”
InfluentialEpithelial–immune crosstalk in health and disease
Rosenblum, D., & Naik, S. (2022) · Current Opinion in Genetics & Development · doi:10.1016/j.gde.2022.101910 · Cited by 20 · see citing works
Phan, Q., Lin, J., Solis, N., Eng, M., Swidergall, M., Wang, F., Li, S., Gaffen, S., Chou, T., & Filler, S. (2021) · bioRxiv · doi:10.1128/mbio.02716-21 · Cited by 14 · see citing works
“albicans invades the epithelial cell lining of the oropharynx, stimulating a strong proinflammatory host response that is driven by interleukin-17 (IL-17) and IL-22 signaling, which is initiated from innate lymphocytes and subsequently from the adaptive immune response (9, 10).”
BackgroundSelf-citationMallela, L. S., Sharma, P., Rao, T. S. R. B., & Roy, S. (2021) · Cellular Microbiology · doi:10.1111/cmi.13367 · Cited by 17 · see citing works
Innovative engineering approaches to model host-microbiome interactions in vitro
Azamar, K. M. M., Sudi, S. D., Mohammadalizadeh, Z., Coffin, C., Parker, I., & Porras, A. M. (2025) · Advanced Drug Delivery Reviews · doi:10.1016/j.addr.2025.115677 · Cited by 12 · see citing works
Mucosal Immunity to Gut Fungi in Health and Inflammatory Bowel Disease
Carlson, S. L., Mathew, L., Savage, M., Kok, K. B., Lindsay, J. O., Munro, C. A., & McCarthy, N. E. (2023) · Journal of Fungi · doi:10.3390/jof9111105 · Cited by 15 · see citing works
“These adverse events highlight the intricacies of the relationship between IL-17, C. albicans and IBD pathogenesis.”
BackgroundLiu, L., Li, X., Chen, Y., Li, Y.-Z., Liu, Z., & Duan, Y. (2023) · Journal of Maternal-Fetal & Neonatal Medicine · doi:10.1080/14767058.2023.2253347 · Cited by 12 · see citing works
“Previous studies have implicated aberrant IL-22 signaling in many disorders, mostly through activation of the JAK/STAT3 pathway [27,28].”
BackgroundImmunomodulatory function of chitosan is dependent on complement receptor 3
Wagener, J., Wang, X., Becker, K. L., Aimanianda, V., Valsecchi, I., Gresnigt, M. S., Netea, M. G., Latgé, J., Gow, N. A. R., & van de Veerdonk, F. L. (2025) · The Cell Surface · doi:10.1016/j.tcsw.2025.100146 · Cited by 12 · see citing works
“IL-22, IL-17 and IFN γ are crucial for the host defence against human pathogens (Valeri and Raffatellu, 2016, Aggor et al., 2020, Lionakis, Drummond et al. 2023).”
Epithelial responses to fungal pathogens
Mills, K. A. M., Aufiero, M. A., & Hohl, T. M. (2024) · Current Opinion in Microbiology · doi:10.1016/j.mib.2024.102508 · Cited by 11 · see citing works
When IL-17 gets on your nerves
Iliev, I., Lin, W.-Y., & Gaffen, S. (2023) · Cell · doi:10.1016/j.cell.2022.12.048 · Cited by 11 · see citing works
Self-citationChen, M.-L., Cheng, T., Xu, C., Pan, M., Wu, J.-D., Wang, T.-M., Wu, D.-Q., Yan, G.-M., Wang, C., & Shao, J. (2022) · Virulence · doi:10.1080/21505594.2022.2035066 · Cited by 11 · see citing works
“[25,26,28,76], and the innate immunity are exquisitely modulated by HIF-1α [77].”
BackgroundZhang, W., Zhang, H., Gao, Y., Lei, J., & Suo, C. (2025) · Frontiers in Cellular and Infection Microbiology · doi:10.3389/fcimb.2025.1596688 · Cited by 12 · see citing works
Zhang, J., Wang, A. X., Wu, Y., & Zhang, S. (2022) · Archives of Oral Biology · doi:10.1016/j.archoralbio.2022.105555 · Cited by 13 · see citing works
IL-17-mediated antifungal immunity restricts Candida albicans pathogenicity in the oral cavity
Fróis-Martins, R., Vicente, K. M. D. S., Maufrais, C., Mertens, S., Sertour, N., Sitterlé, E., Bougnoux, M., d’Enfert, C., & LeibundGut‐Landmann, S. (2025) · Nature Microbiology · doi:10.1038/s41564-025-02198-y · Cited by 8 · see citing works
“IL-22 was previously shown to act in synergy with IL-17 in fungal control 29 and to contribute to tissue remodelling during C. albicans colonization 30 .”
Multiple roles for hypoxia inducible factor 1-alpha in airway epithelial cells during mucormycosis
Kavaliauskas, P., Gu, Y., Hasin, N., Graf, K. T., Alqarihi, A., Shetty, A. C., McCracken, C. L., Walsh, T. J., Ibrahim, A. S., & Bruno, V. M. (2024) · Nature Communications · doi:10.1038/s41467-024-49637-8 · Cited by 11 · see citing works
Self-citationOf Mycelium and Men: Inherent Human Susceptibility to Fungal Diseases
Vinh, D. C. (2023) · Pathogens · doi:10.3390/pathogens12030456 · Cited by 10 · see citing works
“The distinct contributions of IL-17 and IL-22 to CMC immunity were shown in the elegant work conducted by the Gaffen lab [36]: IL-17A and IL-17F act on the supra-basal, post-mitotic epithelial cell layers (SEL), whereas IL-22 stimulates the basal, proliferative progenitor cells (BEL).”
Zhou, C., Monin, L., Gordon, R. A., Aggor, F. E. Y., Bechara, R., Edwards, T. N., Kaplan, D. H., Gingras, S., & Gaffen, S. L. (2020) · The Journal of Immunology · doi:10.4049/jimmunol.2000394 · Cited by 14 · see citing works
“protect from acute OPC, we recently found that STAT3 is essential in the oral epithelium (59, 77).”
BackgroundMethodSelf-citationAntifungal immunity: advances in PRR recognition, adaptive responses, and immune-based therapies
Zhou, J., Lu, X., He, R., Du, Y., Zeng, B., Feng, L., Yi, M., Wang, Y., & Wang, C. (2025) · Science China Life Sciences · doi:10.1007/s11427-024-2835-y · Cited by 8 · see citing works
“IL-22 produced by Th17 cells can also bind to the IL-22 receptor of basal epithelial cells, activate downstream STAT3, and promote epithelial cell proliferation and repair during fungal infection (Aggor et al., 2020).”
Inborn Errors of Immunity Causing Pediatric Susceptibility to Fungal Diseases
Olbrich, P., & Vinh, D. C. (2023) · Journal of Fungi · doi:10.3390/jof9020149 · Cited by 10 · see citing works
Insights into the evolution of Candidalysin and recent developments
Konwar, A., Mathur, K., Pandey, S., Bhorali, K., Thakur, A., & Puria, R. (2025) · Archives of Microbiology · doi:10.1007/s00203-025-04414-z · Cited by 7 · see citing works
“The STAT3 transcription factor present in the basal epithelial cells are activated by IL22, which in turn activates IL17 specific gene that replenishes IL 17RA in order to continuously respond to IL17 signals (Aggor et al. 2020).”
Noma, K., Asano, T., Taniguchi, M., Ashihara, K., & Okada, S. (2025) · Immunological Medicine · doi:10.1080/25785826.2025.2488553 · Cited by 7 · see citing works
“It plays a significant role in maintaining and remodeling skin epithelial cells and keratinocytes, which support host immunity against pathogen invasion [139,140].”
Fan, Y., Xie, S., Wang, T., Huang, Y., Zhang, H., Peng, D., Feng, Y., Yang, Y., Zhang, Z., Zhu, Y., et al. (2024) · Cell Reports · doi:10.1016/j.celrep.2024.115057 · Cited by 7 · see citing works
Beute, J. E., Kim, A. Y., Park, J. J., Yang, A., Torres-Shafer, K., Mullins, D., & Sundstrom, P. (2022) · Frontiers in Cellular and Infection Microbiology · doi:10.3389/fcimb.2022.979701 · Cited by 7 · see citing works
Liu, S., Lin, K., Tian, Y., He, Y., Zhang, Z., Li, C., Luo, Y., Liang, Y., Ma, Y., & Deng, W. (2025) · International Immunopharmacology · doi:10.1016/j.intimp.2025.114672 · Cited by 5 · see citing works
Type 17 immune response promotes oral epithelial cell proliferation in periodontitis.
Zhou, Y., Lv, D., Wei, W., Zhou, T., Tang, S., Yang, F., Zhang, J., Jiang, L.-X., Xia, X.-Q., Jiang, Y.-C., et al. (2024) · Archives of Oral Biology · doi:10.1016/j.archoralbio.2024.106005 · Cited by 5 · see citing works
Zhang, M., Li, D., Sun, L., He, Y., Liu, Q., He, Y., & Li, F. (2024) · Mediators of Inflammation · doi:10.1155/mi/4965271 · Cited by 7 · see citing works
“IL-22/STAT3 signaling promotes proliferation of oral basal epithelial cells [63].”
Host defense mechanisms against Candida auris
Pechacek, J., & Lionakis, M. S. (2023) · Expert Review of Anti-infective Therapy · doi:10.1080/14787210.2023.2264500 · Cited by 5 · see citing works
“By contrast, IL-22 and Card9 were dispensable in this setting [26], as opposed to their protective roles during oral and brain candidiasis [55,56], respectively.”
BackgroundSelf-citationTang, J., Li, J., Pan, J.-Y., Shen, X.-Y., Ye, X., Zhou, J., Wang, N., Xie, L., Fuchs, B., Lionakis, M., et al. (2023) · Infection and Immunity · doi:10.1128/iai.00378-22 · Cited by 5 · see citing works
“inflammatory cytokines and enhancing the host’s ability to eliminate pathogens (11).”
BackgroundSelf-citationWhy targeted therapeutics have provided benefit in psoriasis: looking at IL-17 biology
Lanna, C., Lambiase, S., Shumak, R. G., Borselli, C., Cosio, T., Dattola, A., Bianchi, L., & Campione, E. (2022) · Expert Review of Clinical Pharmacology · doi:10.1080/17512433.2022.2130758 · Cited by 5 · see citing works
“HOST DEFENSE ● IL-17A endorses neutrophil cumulation and function, while IL-22 induces proliferation and antimicrobial peptide production by epithelial cells, crucial defense strategies proposed to fight infections ● IL-17 triggers essential antifungal reactions in OECs, including myeloid and lymphoid chemoattractants…”
BackgroundRemodeling mechanisms and intervention strategies of the oral mucosal immune barrier
Wang, Z., Guo, Y., Fan, Y., Li, X., & Shen, W. (2026) · Frontiers in Immunology · doi:10.3389/fimmu.2026.1815513 · Cited by 5 · see citing works
“By contrast, epithelial STAT3 is mainly activated by IL-22 and IL-6 family cytokines, and promotes the survival, proliferation, and metabolic adaptation of epithelial cells, which aid in the restitution of damaged mucosal surface (46).”
Commensal enteric virome regulates intestinal carbohydrate digestion and absorption
Lin, F., Li, L., He, Y., Xu, S., Mo, Q., Cao, W., Fu, A., & Li, W. (2026) · Cell Host & Microbe · doi:10.1016/j.chom.2026.01.019 · Cited by 8 · see citing works
Kaji, E., Nagao, J.-I., Kishikawa, S., Toyonaga, K., Tasaki, S., Iwai, S., Nakagami, M., Iwanuma, A., Ikeda, M., & Tanaka, Y. (2025) · iScience · doi:10.1016/j.isci.2025.112675 · Cited by 4 · see citing works
“6 7 While C. albicans is commonly found in the human gut, 8 mice do not naturally harbor it, 9,10 making them a great model organism to study the role of intestinal C. albicans during OPC.”
IL-17: A Critical Cytokine for Defense against Oral Candidiasis.
Dias, L. D. S., & Lionakis, M. S. (2024) · Journal of Immunology · doi:10.4049/jimmunol.2400510 · Cited by 4 · see citing works
Self-citationRodríguez, D. L., Lindemann-Pérez, E., & Pérez, J. C. (2024) · Molecular Microbiology · doi:10.1111/mmi.15219 · Cited by 4 · see citing works
“IL- IL- 17-mediated immunity (Aggor et al., 2020; Conti et al., 2009; Gladiator et al., 2013), host cell receptors such as EphA2 (Swidergall et al., 2018) and EphA2-EGFR signaling (Swidergall et al., 2021) have all been shown to play important roles.”
BackgroundSaul‐McBeth, J., Dillon, J., Launder, D., Hickey, M. T., Yi, E. M.-C., Daboul, Y., Biswas, P., Salari, E., Parsai, E. I., & Conti, H. R. (2022) · Journal of Fungi · doi:10.3390/jof8050495 · Cited by 4 · see citing works
“Since, after radiation, the oral immune niche is disrupted, the contribution of other cytokines implicated in antifungal responses, such as IL-23, IL-22, and IL-1, will need to be established as well [14,48,50,51].”
BackgroundSelf-citationHost–Candida auris interactions in the skin
Thangamani, S., Balakumar, A., Datta, A., Bryak, G., & Lionakis, M. S. (2026) · PLOS Pathogens · doi:10.1371/journal.ppat.1014075 · Cited by 3 · see citing works
“The type-17 cytokine, IL-22, although critical for protection against C. albicans oral infection, appears dispensable for immunity in the setting of skin C. auris colonization [3,94].”
Self-citationLv, M., Xu, W., Wang, T., Mou, K., Ni, Z., Tu, Q., Zhang, J., Wu, X., Song, S., & Cheng, G. (2026) · Frontiers in Immunology · doi:10.3389/fimmu.2026.1854213 · Cited by 4 · see citing works
Lindemann‐Perez, E., Rodríguez, D. L., & Pérez, J. C. (2024) · mSphere · doi:10.1128/msphere.00282-24 · Cited by 5 · see citing works
“4), in agreement with previous reports that used antibodies (38).”
BackgroundResultHu, Y., Yu, X.-L., Zhang, X., & Ma, L. (2026) · Frontiers in Microbiology · doi:10.3389/fmicb.2026.1798439 · Cited by 2 · see citing works
“…for maintaining epithelial barrier integrity and coordinating antifungal immunity, the precise impact of MeCP2 deficiency on these specific antifungal defense mechanisms in RTT remains to be fully elucidated (Aggor et al., 2020; De Luca et al., 2010; Napoli et al., 2025; Zelante et al., 2009).”
Feng, R., Huang, H., Ma, Q., Gao, W., Chen, X., Yan, X., Wang, F., Zhang, Q., Cao, Y., Zhang, H., et al. (2026) · Journal of Animal Science and Biotechnology/Journal of animal science and biotechnology · doi:10.1186/s40104-026-01401-2 · Cited by 2 · see citing works
Zhang, X., Zeng, X.-C., Zheng, M.-W., Qiu, X.-W., Zhang, F., & Shi, Q.-R. (2026) · Scientific Reports · doi:10.1038/s41598-026-41303-x · Cited by 2 · see citing works
Millet, N., Sekar, J., Solis, N., Miao, J.-L., Millet, A., Aggor, F. E. Y., Wildeman, A., Cook, M. E., Davari, A., Peters, B. M., et al. (2026) · Nature Communications · doi:10.1038/s41467-026-71459-z · Cited by 2 · see citing works
Self-citationImplications of innate lymphoid cells in oral diseases.
Hu, S.-T., Zhou, G., & Zhang, J. (2024) · International Immunopharmacology · doi:10.1016/j.intimp.2024.112122 · Cited by 2 · see citing works
Delving into the adytum of the IL-17 defense pathway.
Hajishengallis, G. (2023) · Cell Host and Microbe · doi:10.1016/j.chom.2023.08.021 · Cited by 2 · see citing works
Fungal Infections in Disorders of Inborn Errors of Immunity
Dhaliwal, M., Thakur, V., Warris, A., Brown, G. D., Pilania, R. K., & Dambuza, I. M. (2026) · Clinical Reviews in Allergy & Immunology · doi:10.1007/s12016-026-09182-2 · Cited by 1 · see citing works
Insights Into the Susceptibility of Fungal Infection and STAT3 Genetic Mutations
Li, F., Liu, X., Li, Y., Wu, J., Dang, N., & Guo, J. (2026) · Mycoses · doi:10.1111/myc.70200 · Cited by 1 · see citing works
“…member of the STAT protein family, STAT3 mediates signal transduction from numerous cytokines and growth factors, thereby exerting critical regulatory functions in diverse physiological and pathological processes such as cell proliferation, differentiation, apoptosis and immune modulation [2, 20].”
Ding, L., Zhang, Y., Zhang, Q.-X., Tang, X., Wang, Y.-Y., Mao, B.-Y., Zhao, J.-X., & Cui, S.-M. (2025) · Probiotics and Antimicrobial Proteins · doi:10.1007/s12602-025-10723-y · Cited by 1 · see citing works
Coleman, B. M., Cook, M. E., Khan, M. R., Vogel, A. K., Wells, A. J., Miao, J., Vyas, S., Taylor, T. C., Aggor, F. E. Y., Ponde, N. O., et al. (2026) · PLoS Pathogens · doi:10.1371/journal.ppat.1014202 · Cited by 1 · see citing works
Self-citationFanning the Flames: IRAK2 Signaling in Differentiated Epithelium Potentiates Skin Inflammation
Castillo, R., Subudhi, I., & Naik, S. (2021) · Journal of Investigative Dermatology · doi:10.1016/j.jid.2021.04.006 · Cited by 1 · see citing works
Theofilou, V., Konkel, J., Nikitakis, N., & Moutsopoulos, N. (2021) · Burket's Oral Medicine · doi:10.1002/9781119597797.ch19 · Cited by 1 · see citing works
A loss-of-function mutation in IL-17F enhances susceptibility of mice to oropharyngeal candidiasis
Zhou, C., Monin, L., Gordon, R. A., Aggor, F. E. Y., Bechara, R., Edwards, T., Kaplan, D., Gingras, S., & Gaffen, S. (2020) · bioRxiv · doi:10.1101/2020.04.09.028027 · Cited by 1
“We have observed that Il17ra-/- mice show impaired recruitment of neutrophils to the oral 13 mucosa following OPC induction (12, 15, 65).”
BackgroundSelf-citationFan, L.-M., Huang, R.-N., Wang, K.-X., Ni, M.-T., Nong, X.-Y., Xie, Z.-M., Fu, B., Mo, L.-J., Lan, Y., Xu, Q.-Q., et al. (2026) · Frontiers in Cellular and Infection Microbiology · doi:10.3389/fcimb.2026.1960578
“Optimal IL-17-mediated immunity to oral mucosal candidiasis also requires epithelial IL-22/STAT3 signaling (Aggor et al., 2020).”
Lubkin, A., Fellows, A. M., Dias, L. D. S., Oikonomou, V., & Lionakis, M. S. (2026) · mBio · doi:10.1128/mbio.02170-26
Self-citationOrdyniec-Kwaśnica, I., Słomiński, B., Lampkowski, M., Kudra, A., & Muszyński, D. (2026) · Frontiers in Immunology · doi:10.3389/fimmu.2026.1862609
Yuan, W.-B., Tan, L., Du, Y.-Y., Xu, T.-T., Du, Z.-C., Wu, L.-P., Cui, D.-X., & Zhao, Q.-R. (2026) · Molecular and Cellular Biochemistry · doi:10.1007/s11010-026-05704-w
“With accelerating globalization and urbanization, the incidence of IBD continues to rise worldwide, particularly in developing countries [ 1 , 2 ].”
IL-22 synergizes with IL-17 to promote mucosal inflammation and bone loss
Li, X., Ye, X., Yu, X., Liu, S., Wang, H., Korostoff, J. M., Saha, G., Lim, J., & Hajishengallis, G. (2026) · The Journal of Immunology · doi:10.1093/jimmun/vkag186
“90 Thus, it appears that the combined action of IL-22 and IL-17 may be advantageous in the context of infection but potentially detrimental in the context of inflammatory disease.”
Sukumaran, K., Giribabu, N., & Salleh, N. (2026) · European Cytokine Network · doi:10.32604/ecn.2026.078477
“…innate lymphoid cell group 3 and T helper 17 cells and signals through IL-22 receptor on epithelial cells, activating JAK1 and TYK2 and phosphorylating signal transducer and activator of transcription 3, driving expression of β -defensin proteins, S100 proteins, and regenerative programmes [18,88].”
Deng, W., Chen, Y., Liu, S., Liu, S., Zhang, K., Wang, D., Yu, Z., Zhao, W., Xu, Y., Wang, X., et al. (2026) · Immunity & Inflammation · doi:10.1007/s44466-026-00041-5 · Cited by 1 · see citing works
“In concordance with IL-17R, IL-22RA is predominantly expressed in non-hemat-opoietic cells, and the interaction between IL-22 and IL-22RA on the K14 + basal epithelial layer is crucial for maintaining the barrier function of oral epithelial cells during OPC [32].”
- Authors
- Aggor, F. E. Y., Break, T. J., Trevejo-Nuñez, G., Whibley, N., Coleman, B. M., Bailey, R. D., Kaplan, D. H., Naglik, J. R., Shan, W., Shetty, A. C., McCracken, C., Durum, S. K., Biswas, P. S., Bruno, V. M., Kolls, J. K., Lionakis, M. S., & Gaffen, S. L.
- Affiliations
- University of Pittsburgh (US)
- National Institutes of Health (US)
- King's College London (GB)
- University of Maryland, Baltimore (US)
- Tulane University (US)
- Corresponding author
- Gaffen, Sarah L.
- ORCID
- Venue
- Science Immunology
- Published
- 2020-06-26
- Volume
- 5
- Issue
- 48
- ISSN
- 2470-9468 (ISSN-L)
- PMC
- PMC7340112
- OpenAlex
- W3034031851
- Cited by
- 119
- References
- 123
- Citations by year
- 2026: 16 · 2025: 20 · 2024: 18 · 2023: 21 · 2022: 24 · 2021: 17 · 2020: 3
- FWCI
- 5.87
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- other-oa
- Locations
- Science Immunology (publishedVersion)
- PubMed (publishedVersion)
- Research Portal (King's College London) (acceptedVersion, other-oa)
- PubMed Central (acceptedVersion)
- Funders
- National Heart, Lung, and Blood Institute (HL135476, HL139930)
- National Institute of Allergy and Infectious Diseases (AI110820, AI107825)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK104680)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (AR071720, AR060744)
- Wellcome (214229_Z_18_Z)
- King’s College Hospital NHS Foundation Trust (IS-BRC-1215-20006)
- National Institute of Dental and Craniofacial Research (DE022550, DE02815)
- Topics
- Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Health Sciences › Medicine › Infectious Diseases › Antifungal resistance and susceptibility
- Keywords
- IL-22, IL-17, STAT3, oral candidiasis, oral epithelium, IL-22RA1, IL-17RA, antifungal immunity, epithelial regeneration, tongue
- MeSH terms
- Interleukin-22, Animals, Candida albicans, Candidiasis, Oral, Epithelial Cells, Female, Interleukins, Male, Mice, Inbred C57BL, Mouth Mucosa, Signal Transduction, Mice, Knockout, Interleukin-17, STAT3 Transcription Factor, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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