著者

Natsuko AIDA Kazuyoshi TAKEDA Susumu NAKAE Hirohisa SAITO Ko OKUMURA Toshifumi AZUMA Tatsukuni OHNO

出版者

Biomedical Research Press

雑誌

Biomedical Research (ISSN:03886107)

巻号頁・発行日

vol.44, no.1, pp.9-16, 2023-01-25 (Released:2023-01-23)

参考文献数

32

被引用文献数

1

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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.

著者

Kenji Matsumoto Hirohisa Saito

出版者

Japanese Society of Allergology

雑誌

Allergology International (ISSN:13238930)

巻号頁・発行日

vol.62, no.3, pp.291-296, 2013 (Released:2013-09-14)

参考文献数

60

被引用文献数

37

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Results from recent epidemiological studies strongly suggest that ingestion of food promotes immune tolerance to food antigens, whereas exposure to food antigens through skin leads to allergic sensitization. A "dual-allergen-exposure hypothesis" has been proposed to explain those findings. However, several other recent studies have demonstrated that some allergic diseases can be successfully treated by recurrent epicutaneous exposure to allergens. At a glance, these two sets of findings seem to be contradictory, but we think they provide important clues for understanding the mechanisms behind the allergy march. Here, we propose that per-"eczema"tous sensitization drives the allergy march, and we introduce results from several published studies in support of this hypothesis. We hope that this review may help in establishment of new strategies for preventing the allergy march in the near future.