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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.
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“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]
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“Recently, neutrophil recruitment through induction of Th17 responses has been mechanistically linked to the pathogenesis of periodontitis [54].”
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“In both human and murine periodontitis, the dysbiosis-driven Th17 response has been shown to contribute to tissue destruction [76].”
The dynamic landscape of T helper cell plasticity and Th17–Treg instability in periodontitis
Lim, Y.-J., & Kim, T. S. (2026) · Experimental & Molecular Medicine · doi:10.1038/s12276-026-01847-4
Periodontal Status in Patients With Oral Lichen Planus: A Case–Control Study
Rupe, C., Scilla, F., Gioco, G., Candian, M., Castagnola, R., Patini, R., Barbato, L., Cairo, F., & Lajolo, C. (2026) · Oral Diseases · doi:10.1111/odi.70522
Stan, A., Munteanu, S. N., Marcu, T., Pleșea-Condratovici, A., Mititelu-Tarțău, L., Bucă, B. R., Romila, A., Pavel, L. L., & Moisei, M. (2026) · Pharmaceuticals · doi:10.3390/ph19111698
The osteoimmune cell atlas of peri‐implantitis: A narrative scoping review
Cafferata, E. A., Sculean, A., & Schwarz, F. (2026) · Periodontology 2000 · doi:10.1111/prd.70095
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
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