Antigen-specific T cell Sensitization is impaired in IL-17-deficient mice, causing suppression of allergic cellular and humoral responses

Antigen-specific T cell Sensitization is impaired in IL-17-deficient mice, causing suppression of allergic cellular and humoral responses
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DOI:
10.1016/s1074-7613(02)00391-6
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发表时间:
2002-09-01
期刊:
影响因子:
32.4
通讯作者:
Iwakura, Y
Iwakura, Y
中科院分区:
医学1区
文献类型:
--
作者:
Nakae, S;Komiyama, Y;Iwakura, Y

文献摘要

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白细胞介素-17(IL-17)是由T细胞产生的促炎细胞因子。IL-17在哮喘患者血清和关节炎患者滑液中的检测结果表明,IL-17与人类疾病有关。在这项研究中,我们产生了IL-17缺陷小鼠,并研究了IL-17在各种疾病模型中的作用。我们发现,接触,迟发型,气道过敏反应,以及T依赖性抗体的产生,显着减少突变小鼠,而IL-17缺乏供体T细胞不影响急性移植物抗宿主反应。结果表明,受损的反应是由过敏原特异性T细胞活化缺陷引起的。我们的研究结果表明,IL-17在激活T细胞在过敏原特异性T细胞介导的免疫反应中起着重要作用。
Interleukin-17 (IL-17) is a proinflammatory cytokine produced by T cells. The involvement of IL-17 in human diseases has been suspected because of its detection in sera from asthmatic patients and synovial fluids from arthritic patients. In this study, we generated IL-17-deficient mice and investigated the role of IL-17 in various disease models. We found that contact, delayed-type, and airway hypersensitivity responses, as well as T-dependent antibody production, were significantly reduced in the mutant mice, while IL-17 deficiency of donor T cells did not affect acute graft-versus-host reaction. The results suggest that impaired responses were caused by the defects of allergen-specific T cell activation. Our findings indicate that IL-17 plays an important role in activating T cells in allergen-specific T cell-mediated immune responses.