University Hopital Zürich, Department of Pathology, Institute of Experimental Immunology, Zürich, Switzerland.
Immunotherapy. 2009 Mar;1(2):199-203. doi: 10.2217/1750743X.1.2.199.
Th17 cells and their proinflammatory signature cytokine, IL-17, have recently replaced Th1 cells to be the essential Th effector population in autoimmune disease. This was based on a similar line of evidence that previously destined Th1 cells to be the sole encephalitogenic Th-cell effector type. However, as for the Th1-effector type before, an increasing amount of evidence is accumulating that questions the pivotal role of Th17 cells in autoimmunity. Recently, four high-impact articles were published that clearly show that Th1 and Th17 cells carry encephalitogenic properties, and dominance of either in an autoimmune setting can confer disease. In two mouse models for autoimmune neuroinflammation, it was suggested that Th1 and Th17 cells act in parallel, both exhibiting a different set of effector mechanisms.
Th17 细胞及其促炎细胞因子白细胞介素-17（IL-17）最近已取代 Th1 细胞，成为自身免疫性疾病中必不可少的 Th 效应细胞群体。这一观点基于类似的证据，此前曾将 Th1 细胞定位为唯一的致脑炎性 Th 细胞效应细胞类型。然而，与之前的 Th1 效应细胞类型一样，越来越多的证据表明 Th17 细胞在自身免疫中的关键作用值得质疑。最近，有 4 篇高影响力的文章发表，清楚地表明 Th1 和 Th17 细胞均具有致脑炎特性，在自身免疫环境中，无论是哪种细胞占优势都可能导致疾病。在两种自身免疫性神经炎症的小鼠模型中，研究表明 Th1 和 Th17 细胞平行作用，均表现出不同的效应机制。
