Jones Andrew, Hawiger Daniel
Department of Molecular Microbiology and Immunology, Saint Louis University School of Medicine, St. Louis, MO, USA.
Front Immunol. 2017 May 9;8:532. doi: 10.3389/fimmu.2017.00532. eCollection 2017.
Defects in regulatory T cells (Treg cells) aggravate multiple sclerosis (MS) after its onset and the absence of Treg cell functions can also exacerbate the course of disease in an animal model of MS. However, autoimmune neuroinflammation in many MS models can be acutely provoked in healthy animals leading to an activation of encephalitogenic T cells despite the induction of immune tolerance in the thymus including thymically produced (t)Treg cells. In contrast, neuroinflammation can be ameliorated or even completely prevented by the antigen-specific Treg cells formed extrathymically in the peripheral immune system (pTreg cells) during tolerogenic responses to relevant neuronal antigens. This review discusses the specific roles of Treg cells in blocking neuroinflammation, examines the impact of peripheral tolerance and dendritic cells on a relevant regulation of neuroinflammation, and explores some of the most recent advances in elucidation of specific mechanisms of the conversion and function of pTreg cells including the roles of CD5 and Hopx in these processes.
调节性T细胞（Treg细胞）缺陷在多发性硬化症（MS）发病后会使其病情加重，并且在MS动物模型中，Treg细胞功能的缺失也会加剧疾病进程。然而，在许多MS模型中，尽管在胸腺中诱导了免疫耐受，包括胸腺产生的（t）Treg细胞，但健康动物仍可能急性引发自身免疫性神经炎症，导致致脑炎T细胞活化。相比之下，在对相关神经元抗原的耐受性反应过程中，在外周免疫系统中胸腺外形成的抗原特异性Treg细胞（pTreg细胞）可改善甚至完全预防神经炎症。本综述讨论了Treg细胞在阻断神经炎症中的特定作用，研究了外周耐受和树突状细胞对神经炎症相关调节的影响，并探讨了在阐明pTreg细胞转化和功能的特定机制方面的一些最新进展，包括CD5和Hopx在这些过程中的作用。
