Suppression of immune induction of collagen-induced arthritis in IL-17-deficient mice
Suppression of immune induction of collagen-induced arthritis in IL-17-deficient mice
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DOI：
10.4049/jimmunol.171.11.6173
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发表时间：
2003-12-01
影响因子：
4.4
通讯作者：
Iwakura, Y
中科院分区：
文献类型：
--
作者：
Nakae, S;Nambu, A;Iwakura, Y
白细胞介素-17是T细胞衍生的促炎细胞因子。这种细胞因子被怀疑参与类风湿性关节炎（RA）的发展，因为这种细胞因子的表达在RA患者的滑膜组织中增加。然而，IL-17在RA发展中的致病作用仍有待阐明。在本研究中，使用IL-17缺陷小鼠（IL-17（-/-）小鼠）检查IL-17缺陷对胶原诱导的关节炎（CIA）模型的影响。我们发现CIA在IL-17（-/-）小鼠中被显著抑制。IL-17负责胶原特异性T细胞的引发和胶原特异性IgG 2a的产生。因此，这些观察结果表明，IL-17通过激活自身抗原特异性细胞和体液免疫应答在CIA的发展中起着至关重要的作用。
Interleukin-17 is a T cell-derived proinflammatory cytokine. This cytokine is suspected to be involved in the development of rheumatoid arthritis (RA) because this cytokine expression is augmented in synovial tissues of RA patients. The pathogenic roles of IL-17 in the development of RA, however, still remain to be elucidated. In this study, effects of IL-17 deficiency on collagen-induced arthritis (CIA) model were examined using IL-17-deficient mice (IL-17(-/-) mice). We found that CIA was markedly suppressed in IL-17(-/-) mice. IL-17 was responsible for the priming of collagen-specific T cells and collagen-specific IgG2a production. Thus, these observations suggest that IL-17 plays a crucial role in the development of CIA by activating autoantigen-specific cellular and humoral immune responses.