爱尔兰都柏林三一学院Kingston H.G. Mills课题组研究发现，白介素-17A（IL-17A）通过募集IL-1β产生促进病原性T细胞的髓样细胞在自身免疫中发挥主要作用。该研究于2020年2月18日发表于国际学术期刊《免疫学》。

他们发现IL-17A缺陷小鼠或用抗IL-17A治疗的小鼠在诱导实验性自身免疫性脑脊髓炎（EAE）时对疾病具有抗性，并引发分泌IL-17的γδT（γδT17）和Th17细胞缺陷。然而，Il17a-/-小鼠来源的T细胞与自身抗原、IL-1β和IL-23体外培养后，在野生型小鼠中诱导EAE。

此外，用IL-1β或IL-17A治疗EAE可回复II17a-/-小鼠的缺陷。重要的是，在II17a-/-小鼠中，产生IL-1β的嗜中性白细胞和炎性单核细胞的动员以及γδT17细胞的活化降低。他们的发现表明，IL-17A在中枢神经系统（CNS）自身免疫中的关键功能是募集分泌IL-1β的髓样细胞，这些细胞引发致病性γδT17和Th17细胞。

据介绍，IL-17A是许多自身免疫性疾病中组织炎症的主要调控子。抗IL-17A是治疗牛皮癣的有效方法，在多发性硬化症的临床试验中也显示出疗效。

附：英文原文

Title: Interleukin-17A Serves a Priming Role in Autoimmunity by Recruiting IL-1β-Producing Myeloid Cells that Promote Pathogenic T Cells

Author: Aoife M. McGinley, Caroline E. Sutton, Sarah C. Edwards, Charlotte M. Leane, Joseph DeCourcey, Ana Teijeiro, John A. Hamilton, Louis Boon, Nabil Djouder, Kingston H.G. Mills

Issue&Volume: February 04, 2020

Abstract: Interleukin-17A (IL-17A) is a major mediator of tissue inflammation in many autoimmunediseases. Anti-IL-17A is an effective treatment for psoriasis and is showing promisein clinical trials in multiple sclerosis. In this study, we find that IL-17A-defectivemice or mice treated with anti-IL-17A at induction of experimental autoimmune encephalomyelitis(EAE) are resistant to disease and have defective priming of IL-17-secreting γδ T(γδT17) cells and Th17 cells. However, T cells from Il17a/ mice induce EAE in wild-type mice following in vitro culture with autoantigen, IL-1β, and IL-23. Furthermore, treatment with IL-1β orIL-17A at induction of EAE restores disease in Il17a/ mice. Importantly, mobilization of IL-1β-producing neutrophils and inflammatory monocytesand activation of γδT17 cells is reduced in Il17a/ mice. Our findings demonstrate that a key function of IL-17A in central nervous system(CNS) autoimmunity is to recruit IL-1β-secreting myeloid cells that prime pathogenicγδT17 and Th17 cells.

DOI: 10.1016/j.immuni.2020.01.002

Source: https://www.cell.com/immunity/fulltext/S1074-7613(20)30029-7