IL-33 deficiency suppresses alveolar bone loss in a ligature-induced periodontitis model
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- AIDA Natsuko
- Department of Biochemistry, Tokyo Dental College Tokyo Dental College Research Branding Project, Tokyo Dental College
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- TAKEDA Kazuyoshi
- Department of Biofunctional Microbiota, Graduate School of Medicine, Juntendo University Laboratory of Cell Biology, Research Support Center, Graduate School of Medicine
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- NAKAE Susumu
- Graduate School of Integrated Sciences for Life, Hiroshima University
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- SAITO Hirohisa
- Department of Allergy and Clinical Immunology, National Research Institute for Child Health and Development
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- OKUMURA Ko
- Department of Biofunctional Microbiota, Graduate School of Medicine, Juntendo University Atopy Research Center, Graduate School of Medicine, Juntendo University
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- AZUMA Toshifumi
- Department of Biochemistry, Tokyo Dental College Tokyo Dental College Research Branding Project, Tokyo Dental College Oral Health Science Center, Tokyo Dental College
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- OHNO Tatsukuni
- Tokyo Dental College Research Branding Project, Tokyo Dental College Department of Biofunctional Microbiota, Graduate School of Medicine, Juntendo University Oral Health Science Center, Tokyo Dental College
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抄録
<p>Interleukin-33 (IL-33) is a member of the IL-1 cytokine family that has been studied primarily in the context of type 2 immune responses. Recent reports suggest that IL-33 also enhances the func- tions of various immune cells and contributes to the development of different inflammatory diseas- es. Interestingly, IL-33 and its receptor ST2 axis exerted either inhibitory or promotional effects on alveolar bone loss in various periodontitis models. Using a mouse model of ligature-induced periodontitis, we found that the levels of mRNAs encoding IL-33 and other inflammatory cyto- kines (IL-1α, IL-1β, IL-6, and TNFα) were augmented in gingival tissues of wild-type (WT) mice, and that the alveolar bone loss amount was lower in IL-33-deficient than WT mice. The numbers and proportions of IFN-γ-producing CD8+ T and regulatory T cells were decreased while those of Th17 cells were increased in the draining lymph nodes of IL-33-deficient mice compared to WT mice. Additionally, the level of RNA encoding an osteoclastogenic molecule, i.e., receptor activa- tor of nuclear factor kappa-B ligand (RANKL), in ligated gingival tissue was higher in IL-33-defi- cient than WT mice. These results suggest that IL-33 is involved in alveolar bone loss in the ligature-induced periodontitis model, although IL-33 may inhibit osteoclast differentiation.</p>
収録刊行物
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- Biomedical Research
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Biomedical Research 44 (1), 9-16, 2023-01-25
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