Diabetes Center of San Diego, La Jolla Institute for Allergy and Immunology, La Jolla, CA 92037, USA.
J Immunol. 2011 Sep 15;187(6):2915-22. doi: 10.4049/jimmunol.1000180. Epub 2011 Aug 10.
Recent studies have shown that IL-17 can contribute beneficially to pathogen defense but also that excessive IL-17 levels are associated with chronic inflammation and autoimmune disorders. To date, the role of IL-17 in viral infections and type 1 diabetes is ambiguous. In this study, we used IL-17A enhanced green fluorescent protein bicistronic reporter mouse strains to analyze in situ production of IL-17A. Upon Klebsiella pneumoniae bacterial infection, CD4(+) and γδ T cells produce IL-17A. In contrast, CD4(+) or CD8(+) T cells do not produce IL-17A in response to acute or protracted viral infection with lymphocytic choriomeningitis virus or during autoimmune diabetes development in the CD8-driven lymphocytic choriomeningitis virus-induced model of type 1 diabetes. We conclude that viral elimination and type 1 diabetes can occur in the absence of detectable IL-17A production, suggesting IL-17A is not essential in these settings.
最近的研究表明，IL-17 可以对病原体防御有益，但过多的 IL-17 水平与慢性炎症和自身免疫性疾病有关。迄今为止，IL-17 在病毒感染和 1 型糖尿病中的作用尚不清楚。在这项研究中，我们使用了 IL-17A 增强型绿色荧光蛋白双顺反子报告鼠系来分析 IL-17A 的原位产生。在肺炎克雷伯菌感染后，CD4(+)和γδ T 细胞产生 IL-17A。相比之下，在急性或慢性淋巴细胞性脉络丛脑膜炎病毒感染或在 CD8 驱动的淋巴细胞性脉络丛脑膜炎病毒诱导的 1 型糖尿病模型中发生自身免疫性糖尿病时，CD4(+)或 CD8(+) T 细胞不会产生 IL-17A。我们得出结论，在没有可检测到的 IL-17A 产生的情况下，也可以发生病毒清除和 1 型糖尿病，这表明在这些情况下 IL-17A 不是必需的。
