ArticleJournal of immunology (Baltimore, Md. : 1950)2016
Mucosal Langerhans Cells Promote Differentiation of Th17 Cells in a Murine Model of Periodontitis but Are Not Required for Porphyromonas gingivalis-Driven Alveolar Bone Destruction.
Article in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 29 citations in OpenAlex.
- Modulation of the Immune-Inflammatory Microenvironment by Implant Material Properties in Peri-Implantitis.International journal of molecular sciences · 2026Review
- The role of the epithelial sentinels, Langerhans cells and γδT cells, in oral squamous cell carcinoma.Periodontology 2000 · 2024Review
- Major Histocompatibility Complex II Expression on Oral Langerhans Cells Differentially Regulates Mucosal CD4 and CD8 T Cells.The Journal of investigative dermatology · 2024Article
- MHC-II presentation by oral Langerhans cells impacts intraepithelial Tc17 abundance andFrontiers in oral health · 2024Article
- Influence of Vitamin D on Periodontal Inflammation: A Review.Pathogens (Basel, Switzerland) · 2023Review
- Langerhans cells shape postnatal oral homeostasis in a mechanical-force-dependent but microbiota and IL17-independent manner.Nature communications · 2023Article
- Early antitumor activity of oral Langerhans cells is compromised by a carcinogen.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Activation of bone marrow-derived dendritic cells and CD4Journal of oral microbiology · 2022Article
- Update on B Cell Response in Periodontitis.Advances in experimental medicine and biology · 2022Article
- Maintaining homeostatic control of periodontal bone tissue.Periodontology 2000 · 2021Review
- Immunomodulation in the Treatment of Periodontitis: Progress and Perspectives.Frontiers in immunology · 2021Review
- Oral Microbes and Mucosal Dendritic Cells, "Spark and Flame" of Local and Distant Inflammatory Diseases.International journal of molecular sciences · 2020Review
- Infectious Triggers in Periodontitis and the Gut in Rheumatoid Arthritis (RA): A Complex Story About Association and Causality.Frontiers in immunology · 2020Review
- Transient Expression of IL-17A in Foxp3 Fate-Tracked Cells inFrontiers in immunology · 2020Article
- Fetal Weight Outcomes in C57BL/6J and C57BL/6NCrl Mice after Oral Colonization withInfection and immunity · 2019Article
- Mucosal Immunity and the FOXO1 Transcription Factors.Frontiers in immunology · 2019Review
- Cre-loxP Reporter Mouse Reveals Stochastic Activity of theFrontiers in immunology · 2019Article
- Sequential BMP7/TGF-β1 signaling and microbiota instruct mucosal Langerhans cell differentiation.The Journal of experimental medicine · 2018Article
- Revisiting the Page & Schroeder model: the good, the bad and the unknowns in the periodontal host response 40 years later.Periodontology 2000 · 2017Review
- Genes Critical for Developing Periodontitis: Lessons from Mouse Models.Frontiers in immunology · 2017Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Periodontitis is a chronic oral inflammatory disease affecting one in five individuals that can lead to tooth loss. CD4(+) Th cells activated by a microbial biofilm are thought to contribute to the destruction of alveolar bone surrounding teeth by influencing osteoclastogenesis through IL-17A and receptor activator for NF-κB ligand effects. The relative roles of mucosal Ag presentation cells in directing Th cell immune responses against oral pathogens and their contribution to destruction of alveolar bone remain unknown. We tested the contribution of mucosal Langerhans cells (LCs) to alveolar bone homeostasis in mice following oral colonization with a well-characterized human periodontal pathogen, Porphyromonas gingivalis We found that oral mucosal LCs did not protect from or exacerbate crestal alveolar bone destruction but were responsible for promoting differentiation of Th17 cells specific to P. gingivalis. In mice lacking LCs the Th17 response was suppressed and a Th1 response predominated. Bypassing LCs with systemic immunization of P. gingivalis resulted in a predominantly P. gingivalis-specific Th1 response regardless of whether LCs were present. Interestingly, we find that in vivo clonal expansion of P. gingivalis-specific Th cells and induced regulatory T cells does not depend on mucosal LCs. Furthermore, destruction of crestal alveolar bone induced by P. gingivalis colonization occurred regardless of the presence of mucosal LCs or P. gingivalis-specific Th17 cells. Our data indicate that both LCs and Th17 cells are redundant in contributing to alveolar bone destruction in a murine model of periodontitis.
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