The DOI matches its Crossref record; 58 of the 58 references it cites were found in a registry or an index.
A dysbiotic microbiome triggers T H 17 cells to mediate oral mucosal immunopathology in mice and humans
Open accessAbstract
Combined patient and animal model studies implicate microbiota-triggered T H 17 cells as disease drivers and therapeutic targets in periodontitis.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“Studies using germ‐free mice have also been employed in the context of the oral microbiome, demonstrating the role of diabetes in disrupting the equilibrium of the oral microbiota50 and confirming the role of the oral microbiota in periodontal disease pathogenesis.51, 52”
From The oral microbiome: Role of key organisms and complex networks in oral health and disease (2021) · cites this paper as [52]
In the citing paper
“In line with the role of oral mucosa as a physiological barrier, the functions of immune networks within this mucosa reflect the site‐specific challenges faced within the oral cavity. For example, they contribute to homeostasis in response to masticatory forces and trigger immune responses to the development of pathologic microbial communities.52, 53”
From The oral microbiome: Role of key organisms and complex networks in oral health and disease (2021) · cites this paper as [52]
In the citing paper
“Microbial dysbiosis is also necessary for additional inflammatory responses characteristic of periodontal disease, including local expansion of pathologic interleukin‐17+/CD4+ T‐helper (T‐helper 17) cells.52”
From The oral microbiome: Role of key organisms and complex networks in oral health and disease (2021) · cites this paper as [52]
In the citing paper
“The importance of commensal species to pathogenesis is further demonstrated by the requirement for commensal microbial communities in the instigation of disease by periodontal pathogens.51, 52”
From The oral microbiome: Role of key organisms and complex networks in oral health and disease (2021) · cites this paper as [52]
In the citing paper
“homeostatic T‐helper 17 cells were found to be induced by mechanical stimuli in a microbiome‐independent manner, whereas periodontitis‐associated T‐helper 17 cells were found to accumulate in a microbiome‐dependent manner and to require both interleukin‐6 and interleukin‐23.”
From The oral microbiome: Role of key organisms and complex networks in oral health and disease (2021) · cites this paper as [52]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Induction of Intestinal Th17 Cells by Segmented Filamentous Bacteria
Ivanov, I. I., Atarashi, K., Manel, N., Brodie, E. L., Shima, T., Karaoz, U., Wei, D., Goldfarb, K. C., Santee, C. A., Lynch, S. V., et al. (2009) · Cell · doi:10.1016/j.cell.2009.09.033 · Cited by 4,554 · cited 1×
“Microbial induction of TH17 cells has been well documented at various other barrier sites, including the lower GI (32) and skin (33).”
Periodontitis: from microbial immune subversion to systemic inflammation
Hajishengallis, G. (2015) · Nature Reviews Immunology · doi:10.1038/nri3785 · Cited by 3,046 · cited 2×
“To date, the pathogenic drivers of exaggerated destructive inflammation are incompletely understood, and treatment largely aims at reduction of microbial stimulation rather than at targeting of specific immune pathways through hostmodulation therapies (2).”
Self-citationPeriodontitis: a polymicrobial disruption of host homeostasis
Darveau, R. P. (2010) · Nature Reviews Microbiology · doi:10.1038/nrmicro2337 · Cited by 1,688
The IL-23-IL-17 immune axis: from mechanisms to therapeutic testing
Gaffen, S. L., Jain, R., Garg, A. V., & Cua, D. J. (2014) · Nature reviews. Immunology · doi:10.1038/nri3707 · Cited by 1,585
Update on Prevalence of Periodontitis in Adults in the United States: NHANES 2009 – 2012
Eke, P., Dye, B., Wei, L., Slade, G., Thornton-Evans, G., Borgnakke, W., Taylor, G., Page, R., Beck, J., & Genco, R. (2015) · The Journal of Periodontology · doi:10.1902/jop.2015.140520 · Cited by 1,442
Targeting IL-17 and TH17 cells in chronic inflammation
Miossec, P., & Kolls, J. K. (2012) · Nature Reviews Drug Discovery · doi:10.1038/nrd3794 · Cited by 1,414
Homeostatic Immunity and the Microbiota
Belkaid, Y., & Harrison, O. J. (2017) · Immunity · doi:10.1016/j.immuni.2017.04.008 · Cited by 1,261 · cited 1×
“DISCUSSION At mucosal barrier sites, the local immune system is tasked with the delicate act of maintaining a dynamic balance between host and environmental stimuli (26).”
Self-citationSTAT3 Mutations in the Hyper-IgE Syndrome
Holland, S. M., DeLeo, F. R., Elloumi, H. Z., Hsu, A. P., Uzel, G., Brodsky, N. N., Freeman, A. F., Demidowich, A. P., Davis, J., Turner, M. L. C., et al. (2007) · New England Journal of Medicine · doi:10.1056/nejmoa073687 · Cited by 1,233
Self-citationInduction and molecular signature of pathogenic TH17 cells
Lee, Y., Awasthi, A., Yosef, N., Quintana, F. J., Xiao, S., Peters, A., Wu, C., Kleinewietfeld, M., Kunder, S., Hafler, D. A., et al. (2012) · Nature Immunology · doi:10.1038/ni.2416 · Cited by 1,174 · cited 2×
“In human lesions of periodontitis, we document an expansion of TH17 cells that secrete cytokines associated with pathogenic activity (10, 30) and are predominantly resident memory TH17 cells (31).”
Impaired TH17 cell differentiation in subjects with autosomal dominant hyper-IgE syndrome
Milner, J. D., Brenchley, J. M., Laurence, A., Freeman, A. F., Hill, B. J., Elias, K. M., Kanno, Y., Spalding, C., Elloumi, H. Z., Paulson, M. L., et al. (2008) · Nature · doi:10.1038/nature06764 · Cited by 1,157
Self-citation
Flagged first, then by citations
Cited by
Sorted by citations
Items 201–300 of 381
Innovative biomaterials for the treatment of periodontal disease
Zhu, Y. X., Chen, T., Goh, C. M., & Shrestha, A. (2023) · Frontiers in Dental Medicine · doi:10.3389/fdmed.2023.1163562 · Cited by 20
“A murine experimental periodontitis model demonstrated that TH17 cells and the accumulation of neutrophils were necessary for inflammatory tissue destruction (94).”
BackgroundCommensal gut bacterium critically regulates alveolar bone homeostasis
Hathaway‐Schrader, J. D., Carson, M. D., Gerasco, J. E., Warner, A. J., Swanson, B. A., Aguirre, J. I., Westwater, C., Liu, B., & Novince, C. M. (2021) · Laboratory Investigation · doi:10.1038/s41374-021-00697-0 · Cited by 17
Peluso, G., Tian, E., Abusleme, L., Munemasa, T., Mukaibo, T., & Hagen, K. G. T. (2020) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(17)49899-1 · Cited by 17
Self-citationAlveolar Bone Protection by Targeting the SH3BP2-SYK Axis in Osteoclasts
Kittaka, M., Yoshimoto, T., Schlosser, C., Rottapel, R. K., Kajiya, M., Kurihara, H., Reichenberger, E., & Ueki, Y. (2019) · Journal of Bone and Mineral Research · doi:10.1002/jbmr.3882 · Cited by 18
“(8) TH17 cells also function as an osteoclastogenic helper T-cell subset in inflammatory bone destruction.”
BackgroundBhaskaran, N., Schneider, E., Faddoul, F., da Silva, A. P., Asaad, R. J., Talla, A., Greenspan, N. S., Levine, A. D., McDonald, D. J., Karn, J., et al. (2021) · Nature Communications · doi:10.1038/s41467-021-25340-w · Cited by 17
Viral infection and antiviral immunity in the oral cavity
Hickman, H. D., & Moutsopoulos, N. M. (2024) · Nature reviews. Immunology · doi:10.1038/s41577-024-01100-x · Cited by 19
“However, when dysregulated, these cells have also been shown to cause inflammation and immunopathology in the common oral disease periodontitis 92,97,98 .”
Self-citationSystemic Th17 response in the presence of periodontal inflammation
Suárez, L. J., Vargas, D. E., Ciódaro, A. R., Arce, R. M., & Roa, N. S. (2020) · Journal of Applied Oral Science · doi:10.1590/1678-7757-2019-0490 · Cited by 16
Gingival transcriptomics of follicular T cell footprints in progressing periodontitis
Ebersole, J. L., Kirakodu, S. S., Orraca, L., González‐Martínez, J., & González, O. A. (2021) · Clinical & Experimental Immunology · doi:10.1111/cei.13584 · Cited by 16
IL-36 Regulates Neutrophil Chemotaxis and Bone Loss at the Oral Barrier
Liu, J., Meng, H., Mao, Y., Zhong, L., Pan, W., & Chen, Q. (2024) · Journal of Dental Research · doi:10.1177/00220345231225413 · Cited by 17
“Neutrophils play a key role in periodontitis (Silva et al. 2021; Williams et al. 2021) as they regulate bone loss (Dutzan et al. 2018).”
BackgroundRegional specialization within the mammalian respiratory immune system
van Konijnenburg, D. P. H., Nigrovic, P. A., & Zanoni, I. (2024) · Trends in Immunology · doi:10.1016/j.it.2024.09.011 · Cited by 17
Single-Cell Analysis of the Periodontal Immune Niche in Type 2 Diabetes
Belkina, A. C., Azer, M., Lee, J. J., Elgaali, H., Pihl, R. M. F., Cleveland, M., Carr, J., Kim, S. W., Habib, C., Hastürk, H., et al. (2020) · Journal of Dental Research · doi:10.1177/0022034520912188 · Cited by 16
“…in PD, including the Th17 T-cell subset (Jagannathan-Bogdan et al. 2011; Moutsopoulos et al. 2012; McLaughlin et al. 2014; Ip et al. 2016; Dutzan et al. 2018; Nicholas et al. 2019), B cells that play roles in PD of obese but not lean mice (Zhu et al. 2014), and myeloid cells (Hatanaka et…”
BackgroundPotential Roles of Oral Microbiota in the Pathogenesis of Immunoglobin A Nephropathy
He, J., Zhou, S., Hou, P., Wang, Y., Gan, T., Li, Y., Liu, Y., Liu, L., Shi, S., Zhu, L., et al. (2021) · Frontiers in Cellular and Infection Microbiology · doi:10.3389/fcimb.2021.652837 · Cited by 16
ILC1s and ILC3s Exhibit Inflammatory Phenotype in Periodontal Ligament of Periodontitis Patients
Li, C., Liu, J., Pan, J., Wang, Y., Shen, L., & Xu, Y. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.708678 · Cited by 16
“Previous reports have shown that inflammatory cytokines IL17A and IFN-g are implicated in driving the pathogenesis of periodontitis and consequent bone and tooth loss (32).”
Oral Pathobionts Promote MS-like Symptoms in Mice
Zhou, L., Lin, W.-Z., Liu, T., Chen, B.-Y., Meng, X.-Q., Li, Y., Du, L., Liu, Y., Qian, Y.-C., Zhu, Y., et al. (2022) · Journal of Dental Research · doi:10.1177/00220345221128202 · Cited by 16
“Th17 cells are significantly increased in periodontal tissues—the predominant site of lesion in response to local stimulus of dysbiotic oral microbiota (Dutzan et al. 2018).”
BackgroundStandardized studies of the oral microbiome: From technology‐driven to hypothesis‐driven
Gao, C., Li, X., Zhao, X., Yang, P., Wang, X., Chen, X., Chen, N., & Chen, F. (2022) · iMeta · doi:10.1002/imt2.19 · Cited by 15
Probiotics During the Therapeutic Management of Periodontitis
Furlaneto, F. A. C., Ishikawa, K., Messora, M. R., & Mayer, M. P. A. (2022) · Advances in experimental medicine and biology · doi:10.1007/978-3-030-96881-6_19 · Cited by 20
Abdullameer, M. A., & Abdulkareem, A. A. (2023) · Health Science Reports · doi:10.1002/hsr2.1103 · Cited by 17
“Data from experimental animal models showed that mice lacking Th17 cells experienced decreased bone loss and inflammation during periodontitis.(15,16) This suggests that IL‐17 is likely contributing to the loss of alveolar bone through increasing the expression of receptor activator of nuclear factor‐κB ligand (RANKL)…”
Zhao, D., Yang, R., Wei, H.-X., Yang, K., Yang, Y., Wang, N.-X., Zhang, Q., Chen, F., & Zhang, T. (2025) · Frontiers in Immunology · doi:10.3389/fimmu.2024.1449411 · Cited by 18
Natural Killer T (NKT) Cells and Periodontitis: Potential Regulatory Role of NKT10 Cells
Melgar-Rodríguez, S. A., Cafferata, E. A., Díaz, N., Peña, M. A., González, L., Rojas, C., Sierra‐Cristancho, A., Cárdenas, A. M., Díaz-Zúñiga, J. A., & Vernal, R. (2021) · Mediators of Inflammation · doi:10.1155/2021/5573937 · Cited by 14
A reappraisal of microbiome dysbiosis during experimental periodontitis
Arce, M., Endo, N., Dutzan, N., & Abusleme, L. (2022) · Molecular Oral Microbiology · doi:10.1111/omi.12382 · Cited by 14
“Interestingly, the microbialprofileobservedinthosestudiesthatperformedlongitudinal sampling (Dutzan et al., 2018; Kitamoto et al., 2020; Tsukasaki et al., 2018) 4), albeit at much lower abundance.”
BackgroundMethodInfluentialSelf-citationKoshy, B., Rees, J. S., FARNELL, D. J. J., Wei, X., & Waddington, R. J. (2019) · Journal of Dentistry · doi:10.1016/j.jdent.2019.04.009 · Cited by 15
“Triggered by a dysbiotic microbiome, an increase in Th17 cells and neutrophils has been reported associated with inflammatory periodontal tissue destruction and defects in these cells resulted in reduced bone loss 40 .”
BackgroundBao, K., Li, X., Kajikawa, T., Abe, T., Selevsek, N., Grossmann, J., Hajishengallis, G., & Bostancı, N. (2019) · PROTEOMICS · doi:10.1002/pmic.201900253 · Cited by 14
Self-citationAntimicrobial‐induced oral dysbiosis exacerbates naturally occurring alveolar bone loss
Swanson, B. A., Carson, M. D., Hathaway‐Schrader, J. D., Warner, A. J., Kirkpatrick, J. E., Corker, A., Alekseyenko, A. V., Westwater, C., Aguirre, J. I., & Novince, C. M. (2021) · The FASEB Journal · doi:10.1096/fj.202101169r · Cited by 13
Peluso, G., Tian, E., Abusleme, L., Munemasa, T., Mukaibo, T., & Hagen, K. G. T. (2019) · Journal of Biological Chemistry · doi:10.1074/jbc.ra119.009807 · Cited by 13
“Similar to previous studies in mice and humans (6, 42), the microbial community structure of WT animals was stable over time, as no significant differences were found between 8- and 12-week samples for either male or female animals (Fig.”
ResultSelf-citationMicrobiome-mediated regulation of anti-fungal immunity
Zelante, T., Costantini, C., & Romani, L. R. (2020) · Current Opinion in Microbiology · doi:10.1016/j.mib.2020.05.002 · Cited by 14
“Indeed, dysbiosis might represent a key factor for the risk of developing obesity, autoimmunity, cancer and infections [30].”
BackgroundMesenchymal Stromal/Stem Cells-Derived Exosomes as an Antimicrobial Weapon for Orodental Infections
Jafari, N., Khoradmehr, A., Moghiminasr, R., & Habashi, M. S. (2022) · Frontiers in Microbiology · doi:10.3389/fmicb.2021.795682 · Cited by 12
Zhang, J., Wang, A. X., Wu, Y., & Zhang, S. (2022) · Archives of Oral Biology · doi:10.1016/j.archoralbio.2022.105555 · Cited by 14
Therapeutic delivery of CCL2 modulates immune response and restores host–microbe homeostasis
Shehabeldin, M., Gao, J., Cho, Y., Chong, R., Tabib, T., Li, L., Smardz, M., Gaffen, S. L., Diaz, P. I., Lafyatis, R., et al. (2024) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2400528121 · Cited by 12
Self-citationZhou, H., Li, Y., Chen, X., Miao, D., Zhang, L., Cao, R., Li, Q., & Liu, T. (2024) · International Dental Journal · doi:10.1016/j.identj.2024.10.022 · Cited by 12
Triggering mouth-resident antiviral CD8+ T cells potentiates experimental periodontitis
Saavedra, F. M., Brotto, D. B., Joag, V., Matson, C. A., Nesmiyanov, P. P., Herzberg, M. C., Vezys, V., Masopust, D., & Stolley, J. M. (2025) · Mucosal Immunology · doi:10.1016/j.mucimm.2025.02.003 · Cited by 12
“Exacting studies employing the LIP model showed that, in response to a LIP-associated dysbiotic microbiota, gingival-resident ‘T helper 17 ′ CD4 + T cells (T H 17) and PMNs are critical for alveolar bone loss 15 .”
Kim, O., Park, K., Jin, H., Cho, Y., Kim, Y. S., Kwon, S., Koh, J., Ju, J. K., Kee, S., & Park, Y. (2022) · Journal Of Clinical Periodontology · doi:10.1111/jcpe.13648 · Cited by 13
Yarkaç, F. U., Babayiğit, O., & Göktürk, Ö. (2024) · Odontology · doi:10.1007/s10266-024-00907-3 · Cited by 11
“Th17 cell proliferation and IL-17 production play a role in the development of periodontal disease [43, 44].”
Hsiao, P., Huang, R., Huang, L., Chu, C., Dyke, T. E. V., Mau, L., Cheng, C., Sung, C., Weng, P., Wu, Y., et al. (2024) · Journal of Periodontology · doi:10.1002/jper.23-0561 · Cited by 11
The association between periodontal microbial biomarkers and primary therapy outcome
Werner, N., Frasheri, I., Heck, K., Ern, C., Heym, R., Bumm, C. V., & Folwaczny, M. (2024) · Clinical Oral Investigations · doi:10.1007/s00784-024-05904-y · Cited by 10
ICAM1+ gingival fibroblasts modulate periodontal inflammation to mitigate bone loss
Kim, W., Prasongyuenyong, K., Ko, A., Debnath, R., Chen, Z., Zhou, J. X., Shaaf, E., & Ko, K. I. (2024) · Frontiers in Immunology · doi:10.3389/fimmu.2024.1484483 · Cited by 10
Niche rather than origin dysregulates mucosal Langerhans cells development in aged mice
Horev, Y., Salameh, R., Nassar, M., Capucha, T., Saba, Y., Barel, O., Zubeidat, K., Matanes, D., Leibovich, A., Heyman, O., et al. (2020) · Mucosal Immunology · doi:10.1038/s41385-020-0301-y · Cited by 12
Healthy mouth, healthy gut: a dysbiotic oral microbiome exacerbates colitis
Moutsopoulos, N. M., & Konkel, J. E. (2020) · Mucosal Immunology · doi:10.1038/s41385-020-00341-y · Cited by 10
Self-citationTissue-resident memory T cells in antifungal immunity.
LeibundGut-Landmann, S. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.693055 · Cited by 10
“In periodontitis, expansion of Th17 TRMs drives immunopathology in response to local dysbiosis (68).”
BackgroundAcar, B., Gümüş, E., Bulut, S. Ö., Özşin‐Özler, C., Boyraz, M. S., Tan, Ç., Yaz, İ., Özbek, B., Cağdaş, D. N., Saltık‐Temizel, İ. N., et al. (2021) · Journal of Periodontology · doi:10.1002/jper.21-0514 · Cited by 10
Th-Cell Subsets of Submandibular Lymph Nodes in Peri-Implantitis
Zhang, H., Sun, M., Xu, H., & Huang, H. (2024) · Journal of Craniofacial Surgery · doi:10.1097/scs.0000000000009927 · Cited by 9
“21,47 Controlling Th17/Treg imbalance may be the key to break the link between oral and systemic in fl ammatory diseases.”
BackgroundWang, L., Juang, S., Chang, H., He, A.-C., Chen, W.-A., Huang, Y., Dyke, T. E. V., Sheng‐Kai, K., & Chen, Y. (2024) · Journal of Prosthodontic Research · doi:10.2186/jpr.jpr_d_23_00309 · Cited by 9
Insulin-binding protein-5 down-regulates the balance of Th17/Treg
Zhu, M., Han, H., Hu, L., Cao, Y., & Fan, Z. (2022) · Frontiers in Immunology · doi:10.3389/fimmu.2022.1019248 · Cited by 9
“trials suggest that IL−17 inhibition could be beneficial for the treatment of chronic inflammatory diseases, including periodontitis (30, 31).”
BackgroundMesenchymal stem cell–derived extracellular vesicles in periodontal bone repair
Chen, M., Huang, B., & Su, X. (2025) · Journal of Molecular Medicine · doi:10.1007/s00109-025-02513-4 · Cited by 8
Neutrophils linking periodontitis and Alzheimer's disease
Li, J., Liu, L., Xu, C., Zhang, J., & Wang, F. (2025) · Oral Science and Homeostatic Medicine · doi:10.26599/oshm.2025.9610022 · Cited by 8
Neutrophils and periodontitis: From pathological mechanisms to therapeutic opportunities
Si, L., Li, N., & Yang, K. (2025) · International Immunopharmacology · doi:10.1016/j.intimp.2025.115912 · Cited by 8
Oral Microbiota Signatures in the Pathogenesis of Euthyroid Hashimoto’s Thyroiditis
Erdem, M. G., Ünlü, Ö., Ates, F., Karış, D., & Demırci, M. (2023) · Biomedicines · doi:10.3390/biomedicines11041012 · Cited by 8
“In oral cavity infections such as periodontitis, Th17 lymphocytes have been shown to play an important role in shaping the immune response leading to increased development of gingivitis and tooth loss [10].”
BackgroundDissociation of murine oral mucosal tissues for single cell applications
Ikeuchi, T., Akhi, R., Rodriguez, B. C., FRASER, D. D., Williams, D. W., Kim, T. S., Greenwell‐Wild, T., Overmiller, A. M., Morasso, M. I., & Moutsopoulos, N. M. (2023) · Journal of Immunological Methods · doi:10.1016/j.jim.2023.113605 · Cited by 8
Self-citationPinto, R. D., Landi, L., Grassi, G. M., Sforza, N. M., Cairo, F., Citterio, F., Paolantoni, G., D’Aiuto, F., Ferri, C., Monaco, A., et al. (2021) · Oral Diseases · doi:10.1111/odi.14009 · Cited by 10
Okawa, H., Kondo, T., Hokugo, A., Cherian, P., Sundberg, O., Campagna, J. J., Kashemirov, B. A., John, V., Sun, S., Ebetino, F. H., et al. (2022) · Communications Medicine · doi:10.1038/s43856-022-00172-x · Cited by 8
γδT cells in oral tissue immune surveillance and pathology
Chen, Y., Du, J., Liu, Y., Luo, Z., Guo, L., Xu, J., Lü, J., & Liu, Y. (2023) · Frontiers in Immunology · doi:10.3389/fimmu.2022.1050030 · Cited by 7
“N/A Instead of gd17T cells, Th17 cell-derived IL-17 mediates pathology in periodontitis (80)”
BackgroundInfluentialZhou, K., Xie, J., Su, Y., & Fang, J. (2023) · Biotechnology and Genetic Engineering Reviews · doi:10.1080/02648725.2023.2183617 · Cited by 9
“Currently, chronic periodontitis is one of the most common oral disorders (Dutzan et al., 2018).”
Kendlbacher, F. L., Bloch, S., Hager‐Mair, F. F., Schäffer, C., & Andrukhov, O. (2024) · Archives of Oral Biology · doi:10.1016/j.archoralbio.2024.106004 · Cited by 7
Pyroptosis: A major trigger of excessive immune response in the gingiva
Xiang, X., Zhang, J., & Yue, Y. (2024) · Oral Diseases · doi:10.1111/odi.15013 · Cited by 7
Periodontitis and Diabetes Differentially Affect Inflammation in Obesity
Calvo, S. S.-C., Saraswat, S., Hastürk, H., Dawson, D. R., Zhang, X. D., & Nikolajczyk, B. S. (2024) · Journal of Dental Research · doi:10.1177/00220345241280743 · Cited by 7
Osteocyte dysregulation in periodontitis: Pathological mechanisms and therapeutic potential
Si, L., Tian, X., Tian, L., & Yang, K. (2025) · Cellular Signalling · doi:10.1016/j.cellsig.2025.112062 · Cited by 8
Autoimmunity and Periodontitis
Costalonga, M., Thumbigere‐Math, V., & Herzberg, M. (2026) · Journal of Periodontal Research · doi:10.1111/jre.70058 · Cited by 7
“IL23R polymorphisms are major determinants of IBD risk [193, 194], and increased IL-23/Th17 activity is a consistent feature of periodontitis [195, 196].”
The bidirectional effects and mechanisms of the oral and gut microbiomes: a narrative review
Huo, T., Huang, X., Liao, J., Zhang, H., Hu, L., & Xie, M. (2026) · Frontiers in Immunology · doi:10.3389/fimmu.2026.1697413 · Cited by 8
“Th17 cells expansion, dependent on IL-6 and IL-23 signaling, promotes tissue destruction and may enhance colonization of oral pathogens within epithelial niches (127).”
The impact of the soluble epoxide hydrolase cascade on periodontal tissues
Abdalla, H. B., & Dyke, T. E. V. (2023) · Frontiers in Dental Medicine · doi:10.3389/fdmed.2023.1129371 · Cited by 7
Bite-sized immunology; damage and microbes educating immunity at the gingiva
Konkel, J. E., Cox, J. R., & Wemyss, K. (2024) · Mucosal Immunology · doi:10.1016/j.mucimm.2024.07.004 · Cited by 8
Single-cell RNA-seq reveals a resolving immune phenotype in the oral mucosa
Cantalupo, P. G., Diacou, A., Park, S., Soman, V., Chen, J., Glenn, D., Chandran, U. R., & Clark, D. R. (2024) · iScience · doi:10.1016/j.isci.2024.110735 · Cited by 7
Effect of interleukin‐17 on periodontitis development: An instrumental variable analysis
Baumeister, S., Holtfreter, B., Reckelkamm, S. L., Hagenfeld, D., Kocher, T., Alayash, Z., Ehmke, B., Baurecht, H., & Nolde, M. (2023) · Journal of Periodontology · doi:10.1002/jper.22-0365 · Cited by 7
NET histones inflame periodontitis
Papayannopoulos, V. (2023) · The Journal of Experimental Medicine · doi:10.1084/jem.20230783 · Cited by 7
A Summary of the Fifth Annual Virology Education HIV Microbiome Workshop
Sherrill-Mix, S. A., Connors, K. A., Aldrovandi, G. M., Brenchley, J. M., Boucher, C. A., Bushman, F. D., Collman, R. G., Dandekar, S., Klatt, N. R., Lagenaur, L. A., et al. (2020) · AIDS Research and Human Retroviruses · doi:10.1089/aid.2020.0121 · Cited by 6
“However, during disease, Th17 expansion appears to be dependent on the microbiome since antibiotic treatment (particularly those affecting the gram-negative anaerobic bacteria) reduces Th17 accumulation.(43) Small molecule inhibitors or genetic knockout of Th17 cells reduced inflammation and bone loss in a mouse model…”
Li, L., Hayashi-Okada, Y., Falkner, K. L., Shimizu, Y., Zambon, J. J., Kirkwood, K. L., Schifferle, R. E., Genco, R. J., & Diaz, P. I. (2025) · Journal of Periodontology · doi:10.1002/jper.24-0141 · Cited by 6
Self-citationHidalgo, M. A. R., Caldeira, F. I. D., Orrico, S. R. P., Leite, F. R. M., & Scarel‐Caminaga, R. M. (2025) · Biomedicines · doi:10.3390/biomedicines13082028 · Cited by 6
Ji, R., Zhao, X., Zhen, C., Ge, Y., Wu, Z., & Wang, X. (2025) · Biology · doi:10.3390/biology14101393 · Cited by 6
Alterations of the nasal and oral microbiota in multiple sclerosis
Li, S., Montini, F., Song, A., Willocq, V., Chan, E., Shamah, R., Weiner, M., Glanz, B. I., Weiner, H. L., & Cox, L. M. (2025) · EBioMedicine · doi:10.1016/j.ebiom.2025.105959 · Cited by 6
“20,21 Porphyromonas gingivalis, the major etiological agent of chronic periodontitis, worsened EAE and induced proinflammatory responses of CNS glial cells.”
Li, X., Wang, H., Schmidt, C. Q., Ferreira, V. P., Yancopoulou, D., Mastellos, D. C., Lambris, J. D., & Hajishengallis, G. (2023) · The Journal of Immunology · doi:10.4049/jimmunol.2300242 · Cited by 6
Self-citationWang, J.-J., Cheng-lei, Z., Guo, X., & Yang, C. (2023) · The Journal of Steroid Biochemistry and Molecular Biology · doi:10.1016/j.jsbmb.2023.106347 · Cited by 6
The Oral–Lung Microbiome Axis in Connective Tissue Disease-Related Interstitial Lung Disease
Bongers, K. S., Massett, A., & O’Dwyer, D. N. (2024) · Seminars in Respiratory and Critical Care Medicine · doi:10.1055/s-0044-1785673 · Cited by 7
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., Xia, X., Jiang, Y., et al. (2024) · Archives of Oral Biology · doi:10.1016/j.archoralbio.2024.106005 · Cited by 6
Wu, X., Han, X., Zhu, H., Li, M., Gong, L., Jing, S., Xie, W., Liu, Z., Li, C., & Zhang, Y. (2025) · Journal of Experimental & Clinical Cancer Research · doi:10.1186/s13046-025-03296-9 · Cited by 6
The bidirectional effect of neutrophils on periodontitis model in mice: A systematic review
Liu, S., Chen, Y., Jiang, Y., Du, J., Guo, L., Xu, J., Liu, Y., & Liu, Y. F. (2023) · Oral Diseases · doi:10.1111/odi.14803 · Cited by 7
Origin of Th17 Cells in Type 2 Diabetes-Potentiated Periodontal Disease
Nikolajczyk, B. S., & Dawson, D. R. (2019) · Advances in experimental medicine and biology · doi:10.1007/978-3-030-28524-1_4 · Cited by 6
Zhou, Y., Xie, X., Chen, H., Xu, L., Qiu, C., Shen, H., Zhou, W., & Song, Z. (2025) · Frontiers in Immunology · doi:10.3389/fimmu.2025.1590665 · Cited by 5
“In animal models, inhibition of STAT3 or ROR g t in CD4 + T cells resulted in the suppression of gingivitis and alveolar bone resorption (34, 35).”
FOXP3+ T Cells—An Emerging Evidence in Periodontitis Therapeutics
Ünsal, R. B. K., Hasuike, A., Badawy, T., Asa’ad, F., Špiljak, B., Yuwanati, M. B., Roganović, J., Liu, Y., Brigi, C., Zambrano, D. M., et al. (2025) · Clinical and Experimental Dental Research · doi:10.1002/cre2.70263 · Cited by 5
Franchin, M., Taira, T. M., Prado, D. D. S., Speck‐Hernandez, C. A., de Andrade, F. B., Abdalla, H. B., Napimoga, M. H., Cunha, T. M., Fukada, S. Y., & Rosalen, P. L. (2022) · Inflammation Research · doi:10.1007/s00011-022-01662-3 · Cited by 5
Mycobacterium tuberculosis: a new hitchhiker in the etiopathogenesis of periodontitis
MohanaSundaram, A., Gohil, N. V., Etekochay, M. O., Patel, P., Gurajala, S., Sathanantham, S. T., Nsengiyumva, M., Kumar, S., & Emran, T. B. (2024) · International Journal of Surgery · doi:10.1097/js9.0000000000001122 · Cited by 8
“In healthy individuals, the oral cavity is maintained by the immune surveillance of CD4+ T cells followed by smaller population of CD8+ T cells and γδ T cells, which helps in maintaining the dynamic balance between bone resorption and osteogenesis [65] .”
BackgroundDanielsen, A. K., Massarenti, L., Minculescu, L., Jensen, P. Ø., Hansen, P. R., Holmstrup, P., Damgaard, C., & Nielsen, C. H. (2024) · Journal of Periodontal Research · doi:10.1111/jre.13317 · Cited by 5
“3,4 Th17 cells, in particular, have been linked directly to osteoclas - togenesis and bone destruction, 5 and their signature cytokine, in - terleukin (IL)- 17, is elevated in the inflamed periodontium 6–10 and gingival crevicular fluid from patients with periodontitis.”
Occlusal trauma aggravates periodontitis through the plasminogen/plasmin system
Liu, X., Li, J., Li, J., Wang, T., Ding, Y. P., Yue, Y., Wang, M., Wei, N., & Hao, L. (2024) · Oral Diseases · doi:10.1111/odi.15081 · Cited by 5
Wang, Y., Li, J., Chen, R., Xu, Q., Wang, D., Mao, C., Xiang, Z., Wu, G., Wu, G., Li, J., et al. (2024) · Microbiological Research · doi:10.1016/j.micres.2024.127930 · Cited by 6
A Potential Role of Phospholipase 2 Group IIA (PLA2-IIA) in P. gingivalis-Induced Oral Dysbiosis
González, O. A., Alves, V. T. E., Alimova, Y. V., Al‐Attar, A., & Ebersole, J. L. (2019) · Advances in experimental medicine and biology · doi:10.1007/978-3-030-28524-1_7 · Cited by 5
Relevant mechanisms of MAIT cells involved in the pathogenesis of periodontitis
Jiang, X., Zhao, Q., Huang, Z., Ma, F., Chen, K., & Li, Z. (2023) · Frontiers in Cellular and Infection Microbiology · doi:10.3389/fcimb.2023.1104932 · Cited by 5
“), inhibits the secretion of antiinflammatory cytokines, such as IL-10 and TGF-b, and accelerates the breakdown of collagen fibres in periodontal tissues (Dutzan et al., 2018).”
BackgroundWomen in immunology: 2020 and beyond
Pierce, S. K., Schwartzberg, P. L., Shah, N. N., & Taylor, N. N. (2020) · Nature Immunology · doi:10.1038/s41590-020-0618-4 · Cited by 5
Th17/IL‐17A Drives Alveolar Bone Loss via the JAK/STAT3‐RANKL Axis in the Periodontal Ligament
Lv, D., Zhang, J., Zhang, Y., Zhou, Y., Wei, W., Zhang, L., Xia, X., Chen, J., Chen, Q., Zhang, P., et al. (2025) · Oral Diseases · doi:10.1111/odi.70154 · Cited by 6
Zhang, Y., Lv, D., Zhang, J., Zhang, L., Wei, W., Yang, D., Jiang, L., Zhou, T., Yang, W., Rao, P., et al. (2025) · International Immunopharmacology · doi:10.1016/j.intimp.2025.115965 · Cited by 4
The Role of Inflammasomes in Chronic Oral Inflammatory Disease and Oral Cancer: A Narrative Review
Al‐Natour, B., Rasheed, I. B., & Karim, I. A. E. (2025) · Dentistry Journal · doi:10.3390/dj13120609 · Cited by 4
“Oral bacterial communities, referred to as oral microbiome, exhibit balanced interaction between mutualistic and pathogenic strains, but dysbiosis elicits an inflammatory response, which results in periodontal disease [52,53].”
Martini, G. R., Hofmann, P., Kamps, A.-K., Weichberger, A., Tikhonova, E., Conroy, A., Pan, X., Namuch, D. M., Rathjens, L., Bergfeld, A., et al. (2026) · Immunity · doi:10.1016/j.immuni.2026.06.013 · Cited by 5
Shang, L., Roffel, S., Slomka, V., D’Agostino, E. M., Métris, A., Buijs, M. J., Brandt, B. W., Deng, D., Gibbs, S., & Krom, B. P. (2025) · Microbiome · doi:10.1186/s40168-025-02033-w · Cited by 4
Cell-Molecular Interactions of Nano- and Microparticles in Dental Implantology
Владимировна, Л. В., Bazikyan, E. A., Демин, Д. Э., Dyachkova, I. G., Zolotov, D. A., Volkov, A. V., Асадчиков, В. Е., Zhigalina, O. M., Khmelenin, D. N., Купцова, Д. Г., et al. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24032267 · Cited by 4
Rodent models for oral microbiome research: considerations and challenges- a mini review
Gopinath, D., Pandiar, D., Li, Z., & Panda, S. (2024) · Frontiers in Oral Health · doi:10.3389/froh.2024.1439091 · Cited by 7
“Immunode fi cient mice tend to harbor more pathogenic microbes in their oral cavity, whereas hyperimmune mice may suppress some bene fi cial microbes (39, 40).”
BackgroundRobust Ligature-Induced Model of Murine Periodontitis for the Evaluation of Oral Neutrophils
Chadwick, J. W., & Glogauer, M. (2020) · Journal of Visualized Experiments · doi:10.3791/59667 · Cited by 4
Ebersole, J. L., Kirakodu, S. S., & Gonzalez, O. (2022) · Molecular Oral Microbiology · doi:10.1111/omi.12377 · Cited by 5
Oral Microbiome Profile of Gingivitis and Periodontitis by Next-Generation SequencingPreprint
Lee, Y., Park, H. J., Jeong, S.-J., Auh, Q., Jung, J., Lee, G., Shin, S., & Hong, J. (2023) · Research Square · doi:10.21203/rs.3.rs-3530768/v1 · Cited by 4
Protein-based double-network hydrogels mimicking oral mucosa
Zhang, Y., Dong, L., Wang, K., Cheng, Y., Gao, T., Yang, J., Shen, X., Cao, Y., & Xue, B. (2025) · Frontiers in Chemistry · doi:10.3389/fchem.2025.1618870 · Cited by 3
“Despite these pharmacological advantages, research on mucosal interfaces has long relied on animal models, primarily due to limited availability of viable human tissues and persistent ethical dilemmas (Dutzan et al., 2018; Gaffen and Moutsopoulos, 2020; Zhang et al., 2021).”
Balancing IL-17–mediated protection and IFN-γ–driven pathology at mucocutaneous barriers
Dias, L. D. S., & Lionakis, M. S. (2025) · Trends in Immunology · doi:10.1016/j.it.2025.09.002 · Cited by 4
Jian, X.-C., Dong, Y.-L., Zhang, M., & Guo, Z.-L. (2026) · International Journal of Nanomedicine · doi:10.2147/ijn.s574786 · Cited by 3
Li, M., Cui, J., Qu, R., Liu, R., Sun, Y., Li, P., Liu, J., Low, A., Huang, X., Gan, F., et al. (2026) · Microbiome · doi:10.1186/s40168-026-02389-7 · Cited by 4
“Th17 cells play a crucial role in inflammation caused by commensal oral bacteria in both mice and humans [48, 49].”
Immune-instructive biomaterials in oral tissue regeneration and therapy
Park, S., Linsley, C. S., Zárubová, J., Wu, B. M., & Li, S. (2026) · Biomaterials · doi:10.1016/j.biomaterials.2026.124232 · Cited by 3
Immune Responses at Host Barriers and Their Importance in Systemic Autoimmune Diseases
Schinnerling, K., Penny, H. A., Soto, J. A., & Melo-González, F. (2023) · Advances in experimental medicine and biology · doi:10.1007/978-3-031-26163-3_1 · Cited by 3
Metadata
- Authors
- Dutzan, N., Kajikawa, T., Abusleme, L., Greenwell-Wild, T., Zuazo, C. E., Ikeuchi, T., Brenchley, L., Abe, T., Hurabielle, C., Martin, D., Morell, R. J., Freeman, A. F., Lazarevic, V., Trinchieri, G., Diaz, P. I., Holland, S. M., Belkaid, Y., Hajishengallis, G., & Moutsopoulos, N. M.
- Affiliations
- Oral Immunity and Inflammation Unit, NIDCR, NIH, Bethesda, MD 20892, USA.
- University of Pennsylvania (US)
- National Institutes of Health (US)
- Genomics and Computational Biology Core, NIDCD, NIH, Bethesda, MD 20892, USA.
- UConn Health (US)
- Corresponding author
- Moutsopoulos, Niki M.
- ORCID
- Dutzan, Nicolas
- Kajikawa, Tetsuhiro
- Abusleme, Loreto
- Zuazo, Carlos E.
- Ikeuchi, Tomoko
- Brenchley, Laurie
- Abe, Toshiharu
- Hurabielle, Charlotte
- Martin, Daniel
- Morell, Robert J.
- Freeman, Alexandra F.
- Lazarevic, Vanja
- Trinchieri, Giorgio
- Diaz, Patricia I.
- Holland, Steven M.
- Belkaid, Yasmine
- Hajishengallis, George
- Moutsopoulos, Niki M.
- Venue
- Science Translational Medicine
- Published
- 2018-10-17
- Volume
- 10
- Issue
- 463
- ISSN
- 1946-6234 (ISSN-L)
- 1946-6242
- PMC
- PMC6330016
- OpenAlex
- W2896857921
- Cited by
- 382
- References
- 58
- Citations by year
- 2026: 38 · 2025: 46 · 2024: 49 · 2023: 46 · 2022: 47 · 2021: 70 · 2020: 57 · 2019: 28 · 2018: 1
- FWCI
- 44.82
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science Translational Medicine (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Fondation pour la Recherche Médicale
- NIAID (IRP)
- NIDCR (Intramural, DE024153, DE026152)
- NCI Intramural
- La Roche-Posay
- CEDEF
- Philippe Foundation
- fondation groupe pasteur mutualité
- Société Française de Dermatologie
- Topics
- Health Sciences › Dentistry › Periodontics › Oral microbiology and periodontitis research
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Keywords
- dysbiosis, oral microbiota, Th17 cells, oral inflammation, periodontitis, oral immunity, targeted therapy
- MeSH terms
- Animals, Bacteria, Bone Resorption, Cell Differentiation, Humans, Inflammation, Mouth Mucosa, Neutrophils, Periodontitis, Interleukin-6, Mice, Interleukin-23, Nuclear Receptor Subfamily 1, Group F, Member 3, Th17 Cells, Microbiota, Dysbiosis
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 ›
Are you an author, or do you see a problem with this page? Request a review
