Gutcher Ilona, Becher Burkhard
Neuroimmunology Unit, Neurology Clinic, University of Zurich, Y44J7 Winterthurerstrasse 190, Zurich 8057, Switzerland.
J Clin Invest. 2007 May;117(5):1119-27. doi: 10.1172/JCI31720.
T cell-mediated autoimmune diseases such as multiple sclerosis and rheumatoid arthritis are driven by autoaggressive Th cells. The pathogenicity of such Th cells has, in the past, been considered to be dictated by their cytokine polarization profile. The polarization of such effector T cells relies critically upon the actions of cytokines secreted by APCs. While Th1 polarization has long been associated with the pathogenesis of autoimmune diseases, recent data obtained in gene-targeted mice and the discovery of Th17 cell involvement in autoimmunity conflict with this hypothesis. In light of these recent developments, we discuss in this review the actions of APC-derived cytokines and their emerging roles in T cell polarization in the context of autoimmune inflammatory responses.
诸如多发性硬化症和类风湿性关节炎等T细胞介导的自身免疫性疾病是由自身攻击性Th细胞驱动的。过去，此类Th细胞的致病性被认为取决于其细胞因子极化谱。这类效应T细胞的极化严重依赖于抗原呈递细胞（APC）分泌的细胞因子的作用。虽然Th1极化长期以来一直与自身免疫性疾病的发病机制相关，但在基因敲除小鼠中获得的最新数据以及Th17细胞参与自身免疫的发现与这一假设相矛盾。鉴于这些最新进展，我们在本综述中讨论了APC衍生的细胞因子的作用及其在自身免疫性炎症反应背景下在T细胞极化中的新作用。
