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
Cited by
Sorted by citations
Local and systemic mechanisms linking periodontal disease and inflammatory comorbidities
Hajishengallis, G., & Chavakis, T. (2021) · Nature Reviews Immunology · doi:10.1038/s41577-020-00488-6 · Cited by 1,871
Self-citationOsteoimmunology: evolving concepts in bone–immune interactions in health and disease
Tsukasaki, M., & Takayanagi, H. (2019) · Nature reviews. Immunology · doi:10.1038/s41577-019-0178-8 · Cited by 812
The oral microbiome: Role of key organisms and complex networks in oral health and disease
Sedghi, L., DiMassa, V., Harrington, A., Lynch, S. V., & Kapila, Y. L. (2021) · Periodontology 2000 · doi:10.1111/prd.12393 · Cited by 755
The role of the microbiota in periodontal disease
Curtis, M. A., Diaz, P. I., & Van Dyke, T. E. (2020) · Periodontology 2000 · doi:10.1111/prd.12296 · Cited by 698
Self-citationThe cytokine network involved in the host immune response to periodontitis
Pan, W., Wang, Q., & Chen, Q. (2019) · International Journal of Oral Science · doi:10.1038/s41368-019-0064-z · Cited by 740
The Intermucosal Connection between the Mouth and Gut in Commensal Pathobiont-Driven Colitis
Kitamoto, S., Nagao‐Kitamoto, H., Jiao, Y., Gillilland, M. G., Hayashi, A., Imai, J., Sugihara, K., Miyoshi, M., Brazil, J. C., Kuffa, P., et al. (2020) · Cell · doi:10.1016/j.cell.2020.05.048 · Cited by 703
“Th17 cells play a key pathogenic role in commensal bacterium-driven inflammation in the oral cavity in mice and humans (Beklen et al., 2007; Cheng et al., 2016; Dutzan et al., 2018; Eskan et al., 2012; Moutsopoulos et al., 2014; Takahashi et al., 2005).”
Human oral mucosa cell atlas reveals a stromal-neutrophil axis regulating tissue immunity
Williams, D. W., Greenwell‐Wild, T., Brenchley, L., Dutzan, N., Overmiller, A. M., Sawaya, A. P., Webb, S., Martı́n, D., Hajishengallis, G., Divaris, K., et al. (2021) · Cell · doi:10.1016/j.cell.2021.05.013 · Cited by 531
Self-citationCurrent understanding of periodontal disease pathogenesis and targets for host‐modulation therapy
Hajishengallis, G., Chavakis, T., & Lambris, J. D. (2020) · Periodontology 2000 · doi:10.1111/prd.12331 · Cited by 558
Self-citationHost–microbiota interactions in immune-mediated diseases
Ruff, W. E., Greiling, T. M., & Kriegel, M. A. (2020) · Nature Reviews Microbiology · doi:10.1038/s41579-020-0367-2 · Cited by 503
The Nexus Between Periodontal Inflammation and Dysbiosis
Dyke, T. E. V., Bartold, P. M., & Reynolds, E. C. (2020) · Frontiers in Immunology · doi:10.3389/fimmu.2020.00511 · Cited by 491
“There is reasonable evidence in other systems that inflammation can cause dysbiosis (4– 7), and there is reasonable evidence that dysbiosis induces inflammation (12).”
BackgroundMicrobial signatures of health, gingivitis and periodontitis
Abusleme, L., Hoare, A., Hong, B., & Diaz, P. I. (2021) · Periodontology 2000 · doi:10.1111/prd.12362 · Cited by 400
Self-citationValm, A. M. (2019) · Journal of Molecular Biology · doi:10.1016/j.jmb.2019.05.016 · Cited by 450
“Additionally, the crucial involvement of TH17 cells in mediating microbiotainduced periodontal disease further supports the central involvement of neutrophils in periodontal disease[39,42].”
BackgroundPeriodontal Disease: The Good, The Bad, and The Unknown
Sedghi, L. M., Bacino, M. S., & Kapila, Y. L. (2021) · Frontiers in Cellular and Infection Microbiology · doi:10.3389/fcimb.2021.766944 · Cited by 409
Maladaptive innate immune training of myelopoiesis links inflammatory comorbidities
Li, X., Wang, H., Yu, X., Saha, G., Kalafati, L., Ioannidis, C., Mitroulis, I., Netea, M. G., Chavakis, T., & Hajishengallis, G. (2022) · Cell · doi:10.1016/j.cell.2022.03.043 · Cited by 346
Self-citationA guide to complement biology, pathology and therapeutic opportunity
Mastellos, D. C., Hajishengallis, G., & Lambris, J. D. (2023) · Nature reviews. Immunology · doi:10.1038/s41577-023-00926-1 · Cited by 351
“Of note, dysbiosis-driven T H 17 cell expansion and associated neutrophil accumulation in periodontal tissues drive immunopathology and inflammatory tissue destruction in both human and experimental mouse periodontal disease 117 .”
Self-citationShen, Z., Kuang, S., Zhang, Y., Yang, M., Qin, W., Shi, X., & Lin, Z. (2020) · Bioactive Materials · doi:10.1016/j.bioactmat.2020.07.002 · Cited by 295
Polarized Macrophages in Periodontitis: Characteristics, Function, and Molecular Signaling
Sun, X., Gao, J., Meng, X. L., Lu, X., Zhang, L., & Chen, R. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.763334 · Cited by 309
“However, excessive IL-17 signaling can lead to inflammation, increasing the production of RANKL in osteoblasts and periodontal ligament fibroblasts, which in turn promotes over-activation of osteoclasts and leads to periodontal bone loss (72, 73); Th17 cell defects are associated with reduced periodontal inflammation…”
BackgroundHajishengallis, G., & Lamont, R. J. (2021) · Periodontology 2000 · doi:10.1111/prd.12371 · Cited by 314
Self-citationAn Overview of Physical, Microbiological and Immune Barriers of Oral Mucosa
Şenel, S. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22157821 · Cited by 268
“Moutsopoulos and his group have comprehensively investigated the role of the microbiota and its metabolites in induction of the local immune cells of the oral mucosal immune system, focusing on the interleukin-17 (IL-17)/T helper 17 (TH17)-dependent pathways that control the two major oral infectious diseases, periodo…”
BackgroundRegulation of host-microbe interactions at oral mucosal barriers by type 17 immunity
Gaffen, S. L., & Moutsopoulos, N. M. (2020) · Science Immunology · doi:10.1126/sciimmunol.aau4594 · Cited by 255
Self-citationMicrobiome Dependent Regulation of Tregs and Th17 Cells in Mucosa
Pandiyan, P., Bhaskaran, N., Zou, M., Schneider, E., Jayaraman, S., & Huehn, J. (2019) · Frontiers in Immunology · doi:10.3389/fimmu.2019.00426 · Cited by 237
“However, dysbiosis can lead excessive Th17 cells and lead to periodontal inflammation (31).”
BackgroundOral polymicrobial communities: Assembly, function, and impact on diseases
Hajishengallis, G., Lamont, R. J., & Koo, H. (2023) · Cell Host & Microbe · doi:10.1016/j.chom.2023.02.009 · Cited by 221
Self-citationOral microbiota: A new view of body health
Lu, M., Xuan, S., & Wang, Z. (2019) · Food Science and Human Wellness · doi:10.1016/j.fshw.2018.12.001 · Cited by 223
New developments in neutrophil biology and periodontitis
Hajishengallis, G. (2019) · Periodontology 2000 · doi:10.1111/prd.12313 · Cited by 203
Self-citationThe role of oral bacteria in inflammatory bowel disease
Read, E., Curtis, M. A., & Neves, J. F. (2021) · Nature Reviews Gastroenterology & Hepatology · doi:10.1038/s41575-021-00488-4 · Cited by 201
Fibrin is a critical regulator of neutrophil effector function at the oral mucosal barrier
Silva, L. M., Doyle, A. D., Greenwell‐Wild, T., Dutzan, N., Tran, C. L., Abusleme, L., Juang, L. J., Leung, J., Chun, E. M., Lum, A. G., et al. (2021) · Science · doi:10.1126/science.abl5450 · Cited by 195
“Oral murine swab samples were obtained and subjected toDNA isolation, amplicon sequencing of the 16S ribosomal RNA (rRNA) V4 region and generated microbiome data were analyzed as previously described (31).”
MethodSelf-citationKim, T. S., Silva, L. M., Theofilou, V. I., Greenwell‐Wild, T., Li, L., Williams, D. W., Ikeuchi, T., Brenchley, L., Core, N. G. A. C. B., Bugge, T. H., et al. (2023) · The Journal of Experimental Medicine · doi:10.1084/jem.20221751 · Cited by 181
“Bone loss was measured as the distance from the cemento-enamel junction to the alveolar bone crest as previously described (Dutzan et al., 2018).”
BackgroundMethodResultInfluentialSelf-citationAberrant 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
“DNA was extracted using the DNeasy Blood and Tissue kit (Qiagen) with modifications as described (59).”
BackgroundMethodSelf-citationMaintaining homeostatic control of periodontal bone tissue
Hathaway‐Schrader, J. D., & Novince, C. M. (2021) · Periodontology 2000 · doi:10.1111/prd.12368 · Cited by 173
Inflammatory Networks Linking Oral Microbiome with Systemic Health and Disease
Kleinstein, S. E., Nelson, K. E., & Freire, M. (2020) · Journal of Dental Research · doi:10.1177/0022034520926126 · Cited by 176
“This interaction between bacteria and the host immune response is critical: it is now understood that host variation in inflammatory genes, including IL-17, can increase the risk of periodontitis and systemic diseases (Bedoya et al. 2013; Dutzan et al. 2018; Borilova Linhartova et al. 2019).”
BackgroundFrailty, aging, and periodontal disease: Basic biologic considerations
Clark, D. L., Kotronia, E., & Ramsay, S. E. (2021) · Periodontology 2000 · doi:10.1111/prd.12380 · Cited by 162
Nanoparticulate cell-free DNA scavenger for treating inflammatory bone loss in periodontitis
Huang, H., Pan, W., Wang, Y., Kim, H. S., Shao, D., Huang, B., Ho, T., Lao, Y., Quek, C. H., Shi, J., et al. (2022) · Nature Communications · doi:10.1038/s41467-022-33492-6 · Cited by 153
Drummond, 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
Self-citationCalvo, S. S.-C., Bharath, L. P., Pugh, G. H., SantaCruz-Calvo, L., Lenin, R. R., Lutshumba, J., Liu, R., Bachstetter, A. D., Zhu, B., & Nikolajczyk, B. S. (2021) · Nature Reviews Endocrinology · doi:10.1038/s41574-021-00575-1 · Cited by 149
Distal Consequences of Oral Inflammation
Konkel, J. E., O’Boyle, C., & Krishnan, S. (2019) · Frontiers in Immunology · doi:10.3389/fimmu.2019.01403 · Cited by 144
“IL-17 is a major driver of disease in periodontitis (130), RA (131), as well as type I diabetes mellitus (132).”
BackgroundPeriodontitis and cardiometabolic disorders: The role of lipopolysaccharide and endotoxemia
Pussinen, P. J., Kopra, E., Pietiäinen, M., Lehto, M. J., Zarić, S., Paju, S., & Salminen, A. (2022) · Periodontology 2000 · doi:10.1111/prd.12433 · Cited by 142
Mucosal immunology of the ocular surface
de Paiva, C. S., Leger, A. J. S., & Caspi, R. R. (2022) · Mucosal Immunology · doi:10.1038/s41385-022-00551-6 · Cited by 145
T and B Cells in Periodontal Disease: New Functions in A Complex Scenario
Figueredo, C. M., Lira-Junior, R., & Love, R. M. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20163949 · Cited by 136
“Also, pharmacologically targeting RORγt, a transcription factor relevant for Th17 differentiation, reduces alveolar bone loss in a murine model of periodontitis [49].”
BackgroundRANKL and osteoimmunology in periodontitis
Tsukasaki, M. (2020) · Journal of Bone and Mineral Metabolism · doi:10.1007/s00774-020-01165-3 · Cited by 132
Penetrating Macrophage-Based Nanoformulation for Periodontitis Treatment
Yan, N. J., Xu, J., Liu, G., Ma, C., Bao, L., Cong, Y., Wang, Z., Zhao, Y., Xu, W., & Chen, C. (2022) · ACS Nano · doi:10.1021/acsnano.2c05923 · Cited by 123
Suárez, L. J., Garzon, H. S., Arboleda, S., & Rodríguez, A. (2020) · Frontiers in Immunology · doi:10.3389/fimmu.2020.591255 · Cited by 122
Clonal hematopoiesis driven by mutated DNMT3A promotes inflammatory bone loss
Wang, H., Divaris, K., Pan, B., Li, X., Lim, J., Saha, G., Barovic, M., Giannakou, D., Korostoff, J. M., Bing, Y., et al. (2024) · Cell · doi:10.1016/j.cell.2024.05.003 · Cited by 122
“2 + Dnmt3a R878H/+ myeloid and T cells (key cells involved in periodontitis 43,44 ) relative to CD45.”
Self-citationExploring the oral-gut linkage: Interrelationship between oral and systemic diseases
Yamazaki, K., & Kamada, N. (2023) · Mucosal Immunology · doi:10.1016/j.mucimm.2023.11.006 · Cited by 117
“Recent studies have highlighted the involvement of IL-17A-producing immune cells, especially Th17 cells reactive to oral pathobionts, in mediating the pathogenesis of periodontitis 63,64 .”
Elashiry, M., Elashiry, M. M., Elsayed, R., Rajendran, M., Auersvald, C., Zeitoun, R., Rashid, M. H., Ara, R., Meghil, M. M., Liu, Y., et al. (2020) · Journal of Extracellular Vesicles · doi:10.1080/20013078.2020.1795362 · Cited by 116
“Th17 effector T cells appear to play a bone degenerative role [13,18,19], while Tregs reportedly attenuate inflammatory bone loss [20,21].”
BackgroundCovid‐19 and oral diseases: Crosstalk, synergy or association?
Brandini, D. A., Takamiya, A. S., Thakkar, P., Schaller, S. J., Rahat, R., & Naqvi, A. R. (2021) · Reviews in Medical Virology · doi:10.1002/rmv.2226 · Cited by 120
“Higher expression of IL‐23 family cytokines is associated with various immunopathologies including Covid‐19 and PD.(72,79,80) Covid‐19 patients with severe disease exhibit pulmonary oedema and lung fibrosis.”
BackgroundÁlvarez, C., Monasterio, G., Cavalla, F., Córdova, L. A., Hernández, M., Heymann, D., Garlet, G. P., Sorsa, T. A., Pärnänen, P., Lee, H., et al. (2019) · Frontiers in Immunology · doi:10.3389/fimmu.2019.01664 · Cited by 116
“Accordingly, patients with autosomaldominant STAT3 deficiency (AD-HIES), are less susceptible to periodontitis (62).”
BackgroundTrained immunity in chronic inflammatory diseases and cancer
Hajishengallis, G., Netea, M. G., & Chavakis, T. (2025) · Nature reviews. Immunology · doi:10.1038/s41577-025-01132-x · Cited by 113
Self-citationPeriodontal inflammation: Integrating genes and dysbiosis
Zhang, S., Yu, N., & Arce, R. M. (2019) · Periodontology 2000 · doi:10.1111/prd.12267 · Cited by 109
Complement-Dependent Mechanisms and Interventions in Periodontal Disease
Hajishengallis, G., Kajikawa, T., Hajishengallis, E., Maekawa, T., Reis, E. S., Mastellos, D. C., Yancopoulou, D., Hastürk, H., & Lambris, J. D. (2019) · Frontiers in Immunology · doi:10.3389/fimmu.2019.00406 · Cited by 95
Self-citationPeriodontitis and Hypertension: Is the Association Causal?
Pinto, R. D., Pietropaoli, D., Aguilera, E. M., D’Aiuto, F., Cześnikiewicz‐Guzik, M., Monaco, A., Guzik, T. J., & Ferri, C. (2020) · High Blood Pressure & Cardiovascular Prevention · doi:10.1007/s40292-020-00392-z · Cited by 103
“Interestingly, the dysbiosis-dependent expansion of TH17 cells appears central also in the development of periodontitis, and people naturally deficient in TH17 cells are less likely to develop periodontitis [55, 56].”
BackgroundPeriodontal ligament stem cells in the periodontitis niche: inseparable interactions and mechanisms
Zhang, Z., Deng, M., Hao, M., & Tang, J. (2021) · Journal of Leukocyte Biology · doi:10.1002/jlb.4mr0421-750r · Cited by 72
DEL-1-Regulated Immune Plasticity and Inflammatory Disorders
Hajishengallis, G., & Chavakis, T. (2019) · Trends in Molecular Medicine · doi:10.1016/j.molmed.2019.02.010 · Cited by 90
Self-citationIL-10 Dampens an IL-17–Mediated Periodontitis-Associated Inflammatory Network
Sun, L., Girnary, M. S., Wang, L.-F., Jiao, Y., Zeng, E., Mercer, K., Zhang, J., Marchesan, J., Yu, N., Moss, K., et al. (2020) · Journal of Immunology · doi:10.4049/jimmunol.1900532 · Cited by 73
Prinz, I., Sandrock, I., & Mrowietz, U. (2019) · The Journal of Experimental Medicine · doi:10.1084/jem.20191397 · Cited by 90
“Experimental models pointed toward a contribution of mechanical stress, i.e., mastication, as well as involvement of dysbiotic oral microbiota to the activation of inflammatory gingival Th17 cells and γδ17 cells (Dutzan et al., 2017, 2018; Krishnan et al., 2018; Wilharm et al., 2019).”
BackgroundImpact of systemic factors in shaping the periodontal microbiome
Teles, F., Wang, Y., Hajishengallis, G., Hastürk, H., & Marchesan, J. T. (2020) · Periodontology 2000 · doi:10.1111/prd.12356 · Cited by 93
Self-citationPhase IIa clinical trial of complement C3 inhibitor AMY-101 in adults with periodontal inflammation
Hastürk, H., Hajishengallis, G., Lambris, J. D., Mastellos, D. C., & Yancopoulou, D. (2021) · Journal of Clinical Investigation · doi:10.1172/jci152973 · Cited by 93
Self-citationAn update on periodontal inflammation and bone loss
Zhang, M., Liu, Y., Afzali, H., & Graves, D. T. (2024) · Frontiers in Immunology · doi:10.3389/fimmu.2024.1385436 · Cited by 93
Periodontal connection with intestinal inflammation: Microbiological and immunological mechanisms
Kitamoto, S., & Kamada, N. (2022) · Periodontology 2000 · doi:10.1111/prd.12424 · Cited by 91
Dysbiosis From a Microbial and Host Perspective Relative to Oral Health and Disease
Cugini, C., Ramasubbu, N., Tsiagbe, V. K., & Fine, D. H. (2021) · Frontiers in Microbiology · doi:10.3389/fmicb.2021.617485 · Cited by 91
“However, all three antibiotic treatments significantly up-regulated the gene expression of pro-inflammatory (IFN-γ, TNF-α, IL-1β, and IL-6) and antiinflammatory cytokines (IL-4, IL-17, IL-23, and IL-10), but varied in fold-change depending on the treatment.”
BackgroundMöller, B., Kollert, F., Sculean, A., & Villiger, P. M. (2020) · Frontiers in Immunology · doi:10.3389/fimmu.2020.01108 · Cited by 82
Fischer, F., Romero, R., Hellhund, A., Linne, U., Bertrams, W., Pinkenburg, O., Eldin, H. S., Binder, K., Jacob, R., Walker, A., et al. (2020) · Gut Microbes · doi:10.1080/19490976.2020.1829962 · Cited by 84
Porphyromonas Gingivalis in the Development of Periodontitis: Impact on Dysbiosis and Inflammation.
Benahmed, A. G., Mujawdiya, P. K., Noor, S., & Gasmi, A. (2022) · PubMed Central · doi:10.22092/ari.2021.356596.1875 · Cited by 78
Regulatory T cell phenotype and anti-osteoclastogenic function in experimental periodontitis
Álvarez, C., Suliman, S., Almarhoumi, R., Vega, M. E., Rojas, C., Monasterio, G., Galindo, M. A., Vernal, R., & Kantarcı, A. (2020) · Scientific Reports · doi:10.1038/s41598-020-76038-w · Cited by 77
Th17 Cells in Periodontitis and Its Regulation by A20
Huang, N., Dong, H., Luo, Y., & Shao, B. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.742925 · Cited by 84
“Inhibiting RORgt and then down-regulating IL-17 expression via GSK805 or curcumin attenuated alveolar bone loss (17, 82).”
BackgroundResultInfluentialSkin Immunity to Dermatophytes: From Experimental Infection Models to Human Disease
Burstein, V. L., Beccacece, I., Guasconi, L., Mena, C. J., Cervi, L., & Chiapello, L. S. (2020) · Frontiers in Immunology · doi:10.3389/fimmu.2020.605644 · Cited by 80
Impact of gut microbiota on gut‐distal autoimmunity: a focus on T cells
Sprouse, M. L., Bates, N. A., Felix, K. M., & Wu, H.-J. J. (2018) · Immunology · doi:10.1111/imm.13037 · Cited by 79
Anticandidal Activities by Lactobacillus Species: An Update on Mechanisms of Action
Vázquez-Muñoz, R., & Dongari‐Bagtzoglou, A. I. (2021) · Frontiers in Oral Health · doi:10.3389/froh.2021.689382 · Cited by 81
“albicans and mitis group streptococci which was first identified experimentally [13, 37], may have clinical implications on Autosomal-Dominant Hyper IgE Syndrome patients, who are susceptible to this oral infection [21].”
BackgroundOral, Tongue-Coating Microbiota, and Metabolic Disorders: A Novel Area of Interactive Research
Li, Y., Cui, J., Liu, Y., Chen, K., Huang, L., & Liu, Y. (2021) · Frontiers in Cardiovascular Medicine · doi:10.3389/fcvm.2021.730203 · Cited by 74
“Changes in the abundance of Enterococcus sp. and Lactobacillus sp. lead to the expansion of Th17 cells and the accumulation of IL-6 and IL-23 (53).”
BackgroundThe Th17/Treg cell balance: crosstalk among the immune system, bone and microbes in periodontitis
Deng, J., Lu, C., Zhao, Q., Chen, K., Ma, S., & Li, Z. (2021) · Journal of Periodontal Research · doi:10.1111/jre.12958 · Cited by 71
Uriarte, S. M., & Hajishengallis, G. (2022) · Immunological Reviews · doi:10.1111/imr.13152 · Cited by 81
Self-citationThe neutrophil–osteogenic cell axis promotes bone destruction in periodontitis
Ando, Y., Tsukasaki, M., Huynh, N. C., Zang, S., Yan, M., Muro, R., Nakamura, K., Komagamine, M., Komatsu, N., Okamoto, K., et al. (2024) · International Journal of Oral Science · doi:10.1038/s41368-023-00275-8 · Cited by 73
Pan, S., Lan, Y., Yang, Y., Zhang, Y., Yu, S., Wang, T., Zhu, Y., Yang, S., Yuan, X., Gao, X. Y., et al. (2025) · ACS Nano · doi:10.1021/acsnano.5c05266 · Cited by 71
Oral Versus Gastrointestinal Mucosal Immune Niches in Homeostasis and Allostasis
Suárez, L. J., Arboleda, S., Angelov, N., & Arce, R. M. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.705206 · Cited by 78
The oral microbiome in autoimmune diseases: friend or foe?
Huang, X., Huang, X., Huang, Y., Zheng, J., Ye, L., Mai, Z., Zhao, X., Cui, L., & Huang, S. (2023) · Journal of Translational Medicine · doi:10.1186/s12967-023-03995-x · Cited by 76
de Molon, R. S., Vernal, R., Oliveira, G. E., Steffens, J. P., Ervolino, E., Theodoro, L. H., van den Beucken, J. J. J. P., & Tetradis, S. (2026) · Bone Research · doi:10.1038/s41413-025-00478-1 · Cited by 85
“63,64 In human periodontitis, active resorptive sites are typically occupied by osteoclasts and their precursors, which are differentiated under the in fl uence of RANKL and pro-in fl ammatory cytokines secreted by immune and stromal cells, including T and B lymphocytes, macrophages, and periodontal…”
Wang, C., Hao, Y., Gianfilippo, R. D., Sugai, J. V., Li, J., Gong, W., Kornman, K. S., Wang, H., Kamada, N., Xie, Y., et al. (2021) · Theranostics · doi:10.7150/thno.57775 · Cited by 67
“The development of peri-implantitis is considered to be driven by the accumulation of bacterial biofilms at the gingival-implant interface in susceptible individuals [1, 9-11].”
BackgroundInterleukin-17 induces pyroptosis in osteoblasts through the NLRP3 inflammasome pathway in vitro
Lei, L., Sun, J., Han, J., Jiang, X., Wang, Z., & Chen, L. (2021) · International Immunopharmacology · doi:10.1016/j.intimp.2021.107781 · Cited by 67
Differential immune cell infiltrations between healthy periodontal and chronic periodontitis tissues
Li, W., Zhang, Z., & Wang, Z. (2020) · BMC Oral Health · doi:10.1186/s12903-020-01287-0 · Cited by 68
Surma, S., Romańczyk, M., Witalińska-Łabuzek, J., Czerniuk, M. R., Łabuzek, K., & Filipiak, K. J. (2021) · Current Hypertension Reports · doi:10.1007/s11906-021-01140-x · Cited by 74
Elsayed, R., Elashiry, M., Liu, Y., El-Awady, A., Hamrick, M., & Cutler, C. W. (2021) · Frontiers in Cellular and Infection Microbiology · doi:10.3389/fcimb.2021.669989 · Cited by 64
“…were to examine whether immune cells, representative of those at the oral mucosal-microbe interface in PD (Cutler and Teng, 2007; Hovav, 2014; Dutzan et al., 2016), are vulnerable to CS in vitro, as induced by the dysbiotic pathogen P. gingivalis (Hajishengallis et al., 2011; Hajishengallis…”
BackgroundPietropaoli, D., Pinto, R. D., Ferri, C., Marzo, G., Giannoni, M., Ortu, E., & Monaco, A. (2019) · Journal Of Clinical Periodontology · doi:10.1111/jcpe.13216 · Cited by 65
Oral Mucositis: An Update on Innate Immunity and New Interventional Targets
Chen, C., Zhang, Q., Yu, W., Chang, B., & Le, A. D. (2020) · Journal of Dental Research · doi:10.1177/0022034520925421 · Cited by 68
“2019), while a dysbiotic microbiome triggers Th17 cells to mediate oral mucosal immunopathology in both mice and humans (Dutzan et al. 2018).”
BackgroundSpecific inhibition of IL‐6 receptor attenuates inflammatory bone loss in experimental periodontitis
Vieira, G. H. A., Rivas, A. C. A., Costa, K., Oliveira, L. F. F., Suzuki, K. T., Messora, M. R., Ricoldi, M. S. T., Almeida, A. L. G., & Taba, M. (2021) · Journal of Periodontology · doi:10.1002/jper.20-0455 · Cited by 67
Rojas, C., García, M. P., Polanco, A., González, L., Sierra‐Cristancho, A., Melgar-Rodríguez, S. A., Cafferata, E. A., & Vernal, R. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.663328 · Cited by 63
Hajishengallis, G., Li, X., Divaris, K., & Chavakis, T. (2022) · Periodontology 2000 · doi:10.1111/prd.12421 · Cited by 70
Self-citationThe Roles of Neutrophils Linking Periodontitis and Atherosclerotic Cardiovascular Diseases
Irwandi, R. A., Chiesa, S. T., Hajishengallis, G., Papayannopoulos, V., Deanfield, J. E., & D’Aiuto, F. (2022) · Frontiers in Immunology · doi:10.3389/fimmu.2022.915081 · Cited by 70
Self-citationRajendran, M., Looney, S. W., Singh, N., Elashiry, M., Meghil, M. M., El‐Awady, A., Tawfik, O. K., Susin, C., Arce, R. M., & Cutler, C. W. (2019) · The Journal of Immunology · doi:10.4049/jimmunol.1900046 · Cited by 63
“Furthermore, it has been demonstrated that dysbiotic microbiome triggers the expansion of Th17 cells in human PD (23).”
BackgroundTongue Coating Bacteria as a Potential Stable Biomarker for Gastric Cancer Independent of Lifestyle
Xu, S., Xiang, C., Wu, J., Teng, Y., Wu, Z., Wang, R., Lu, B., Zhan, Z., Wu, H., & Zhang, J. (2020) · Digestive Diseases and Sciences · doi:10.1007/s10620-020-06637-0 · Cited by 61
Nagao, J.-I., Kishikawa, S., Tanaka, H., Toyonaga, K., Narita, Y., Yasumatsu, K., Tasaki, S., Arita-Morioka, K.-I., Nakayama, J., & Tanaka, Y. (2022) · Cell Reports · doi:10.1016/j.celrep.2022.111314 · Cited by 60
Guided Bone Regeneration Using Barrier Membrane in Dental Applications
Kim, K., Su, Y., Kucine, A. J., Cheng, K., & Zhu, D. (2023) · ACS Biomaterials Science & Engineering · doi:10.1021/acsbiomaterials.3c00690 · Cited by 61
Microbiota-Propelled T Helper 17 Cells in Inflammatory Diseases and Cancer
Bellone, M., Brevi, A., & Huber, S. (2020) · Microbiology and Molecular Biology Reviews · doi:10.1128/mmbr.00064-19 · Cited by 60
“has been shown in individuals with a genetic defect in TH17 cell differentiation (201).”
BackgroundYuh, D., Maekawa, T., Li, X., Kajikawa, T., Bdeir, K. H., Chavakis, T., & Hajishengallis, G. (2020) · Journal of Biological Chemistry · doi:10.1074/jbc.ra120.013024 · Cited by 58
“Specifically, in a model of ligature-induced periodontitis where bone loss is driven by the ligature-associated dysbiotic microbiome (17, 18), ligature removal promotes inflammation resolution in WT mice but not in littermate Del1 mice (4).”
BackgroundMethodSelf-citationActive gingival inflammation is linked to hypertension
Pietropaoli, D., Monaco, A., D’Aiuto, F., Muñoz Aguilera, E., Ortu, E., Giannoni, M., Czesnikiewicz-Guzik, M., Guzik, T. J., Ferri, C., & Del Pinto, R. (2020) · Journal of Hypertension · doi:10.1097/hjh.0000000000002514 · Cited by 56
“The unique contribution of specific and diverse inflammatory pathways in the acute and the chronic settings might be a possible explanation for the observed differences between gingivitis and stable/unstable periodontitis in the reported association [42,43].”
BackgroundT Helper 17 Cells as Pathogenic Drivers of Periodontitis
Dutzan, N., & Abusleme, L. (2019) · Advances in experimental medicine and biology · doi:10.1007/978-3-030-28524-1_9 · Cited by 60
Self-citationTan, J., Dai, A., Pan, L., Zhang, L., Wang, Z., Ke, T., Sun, W., Wu, Y., Ding, P., & Chen, L. (2021) · Journal of Immunology Research · doi:10.1155/2021/9919024 · Cited by 56
RGS12 Drives Macrophage Activation and Osteoclastogenesis in Periodontitis
Yuan, G., Fu, C., Yang, S. T., Yuh, D.-Y., Hajishengallis, G., & Yang, S. (2021) · Journal of Dental Research · doi:10.1177/00220345211045303 · Cited by 57
“Studies showed that the levels of inflammatory factors such as IL1β, IL17, TNFα, and COX2 are related to periodontal tissue damage and bone loss (Kayal 2013; Dutzan et al. 2018).”
BackgroundSelf-citationEpithelial-derived interleukin-23 promotes oral mucosal immunopathology
Kim, T. S., Ikeuchi, T., Theofilou, V. I., Williams, D. W., Greenwell‐Wild, T., June, A., Adade, E. E., Li, L., Abusleme, L., Dutzan, N., et al. (2024) · Immunity · doi:10.1016/j.immuni.2024.02.020 · Cited by 56
Self-citationElashiry, M., Elsayed, R., & Cutler, C. W. (2021) · Cells · doi:10.3390/cells11010115 · Cited by 58
Osteoimmunology in Periodontitis: Local Proteins and Compounds to Alleviate Periodontitis
Sirisereephap, K., Maekawa, T., Tamura, H., Hiyoshi, T., Domon, H., Isono, T., Terao, Y., Maeda, T., & Tabeta, K. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23105540 · Cited by 57
Álvarez, C., Abdalla, H. B., Suliman, S., Rojas, P., Wu, Y., Almarhoumi, R., Huang, R., Galindo, M. A., Vernal, R., & Kantarcı, A. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.664756 · Cited by 55
“CD4 Th17 cells are significantly expanded by the microbial dysbiosis around the tooth, requiring local IL-6 and IL-23 production for their expansion (8, 9).”
Background
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
