白细胞介素-17（IL-17）介导的迟发型超敏反应的发展不受白细胞介素-25（IL-25）表达下调的影响。
Development of IL-17-mediated delayed-type hypersensitivity is not affected by down-regulation of IL-25 expression.
机构信息
Department of Allergy and Immunology, National Research Institute for Child Health and Development, Tokyo, Japan.
出版信息
Allergol Int. 2010 Dec;59(4):399-408. doi: 10.2332/allergolint.10-OA-0218. Epub 2010 Sep 25.
BACKGROUND
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.
METHODS
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.
RESULTS
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.
CONCLUSIONS
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.
背景
IL-25 是 IL-17 家族的一员，可诱导 Th2 细胞分化和 Th2 细胞因子产生，导致 Th2 型免疫应答和疾病的发生，从而抑制 Th1 和 Th17 型免疫应答。
方法
为了阐明 IL-25 在 IL-17 介导的迟发型超敏反应（DTH）发病机制中的作用，用甲基化 BSA（mBSA）对 IL-25 缺陷型小鼠进行致敏，然后用 mBSA 攻击诱导 DTH 反应。基于细胞增殖和细胞因子产生来评估 mBSA 特异性 T 细胞的诱导。根据组织肿胀、组织学和炎症介质表达来评估 DTH 反应。
结果
IL-25 在局部 DTH 病变中的表达明显降低。然而，在 IL-25 缺陷型和野生型小鼠中，mBSA 特异性 Th1、Th2 和 Th17 细胞的诱导以及 mBSA 诱导的 DTH 反应并无差异。
结论
在 mBSA 诱导的 DTH 反应的致敏阶段或激发阶段，IL-25 对于 Th1、Th2 和 Th17 细胞的分化或局部炎症的诱导并非必需。
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