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Development of IL-17-mediated Delayed-Type Hypersensitivity Is Not Affected by Down-Regulation of IL-25 Expression

IL-25, which is a member of the IL-17 family, induces Th2 cell differentiation and Th2 cytokine production, contributing to induction of Th2-type immune responses and diseases, as a result of which it suppresses Th1- and Th17-type immune responses. To elucidate the role of IL-25 in the pathogenesis...

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Bibliographic Details
Published in:Allergology international 2010, Vol.59 (4), p.399-408
Main Authors: Ishii, Akina, Oboki, Keisuke, Nambu, Aya, Morita, Hideaki, Ohno, Tatsukuni, Kajiwara, Naoki, Arae, Ken, Sudo, Hajime, Okumura, Ko, Saito, Hirohisa, Nakae, Susumu
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Language:English
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Summary:IL-25, which is a member of the IL-17 family, induces Th2 cell differentiation and Th2 cytokine production, contributing to induction of Th2-type immune responses and diseases, as a result of which it suppresses Th1- and Th17-type immune responses. To elucidate the role of IL-25 in the pathogenesis of IL-17-mediated delayed-type hypersensitivity (DTH), IL-25-deficient mice were sensitized with methylated BSA (mBSA), and then a DTH reaction was induced by mBSA challenge. mBSA-specific T-cell induction was assessed on the basis of cell proliferation and cytokine production. The DTH reaction was evaluated on the basis of tissue swelling, histology and inflammatory mediator expression. IL-25 expression was markedly reduced in local DTH lesions. However, mBSA-specific Th1, Th2 and Th17 cell induction, and the mBSA-induced DTH reaction were comparable in IL-25-deficient and wild-type mice. IL-25 is not essential for differentiation of Th1, Th2 and Th17 cells in the sensitization phase or induction of local inflammation in the elicitation phase of the mBSA-induced DTH reaction.
ISSN:1323-8930
1440-1592
DOI:10.2332/allergolint.10-OA-0218