Multiple sclerosis (MS) is a neuroinflammatory disease characterized by demyelination of neurons in the central nervous system (CNS) (1). While the ultimate cause of the disease is unknown, MS is commonly considered to be an autoimmune disorder in which autoreactive CD4⁺ T cells are activated by an (unknown) autoantigen presented by antigen-presenting cells (APCs) outside the CNS. Once in the CNS, T cells are activated by microglia-derived or CNS-infiltrating APC, resulting in inflammation and myelin damage. The main T cell subsets causing disease in MS are T helper (Th) 1 and Th17 cells, which produce the proinflammatory cytokines interferon gamma (IFN-γ), interleukin (IL)-17A, and granulocyte–macrophage colony-stimulating factor. Studies in MS patients have shown that IL-17A and IFN-γ levels are increased in T cells isolated from CNS lesions and the cerebrospinal fluid (2, 3). A similar role of Th1 and Th17 cells has been found in the experimental autoimmune encephalomyelitis (EAE) rodent model of MS. The proinflammatory function of Th1 and Th17 cells is kept in check by regulatory T (Treg) cells, a subset of CD4⁺ T cells that express the transcription factor Foxp3 by suppressing effector T cell functions and thus CNS inflammation. Treg cells attenuate the severity of EAE and contribute to recovery from CNS inflammation (4). A report by Othy et al. (5) sheds light on the spatiotemporal interaction of Th17 cells, Treg cells, and APCs and their migration at three different stages of EAE. It also shows how Treg cells modulate Ca²⁺ signals in Th17 cells in the spinal cord.

中文翻译：

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眼见为实：可视化神经炎症不同阶段的免疫细胞和钙信号。

多发性硬化症（MS）是一种神经炎症性疾病，其特征在于中枢神经系统（CNS）中神经元的脱髓鞘作用（1）。虽然疾病的最终原因尚不清楚，但MS通常被认为是一种自身免疫性疾病，其中CD4 ⁺T细胞被CNS外部的抗原呈递细胞（APC）呈递的（未知）自身抗原激活。一旦进入中枢神经系统，T细胞就会被小胶质细胞来源或中枢神经系统浸润的APC激活，从而导致炎症和髓磷脂损伤。引起MS疾病的主要T细胞亚群是T辅助（Th）1和Th17细胞，它们产生促炎细胞因子干扰素γ（IFN-γ），白介素（IL）-17A和粒细胞-巨噬细胞集落刺激因子。已在MS患者的研究表明，IL-17A和IFN-γ水平在从CNS损伤和脑脊髓液（分离的T细胞中增加的2，3）。已在MS的实验性自身免疫性脑脊髓炎（EAE）啮齿动物模型中发现了Th1和Th17细胞的相似作用。Th1和Th17细胞的促炎功能受到调节性T（Treg）细胞的抑制，调节性T细胞是CD4 ⁺ T细胞的一个子集，通过抑制效应T细胞功能和中枢神经系统炎症来表达转录因子Foxp3。Treg细胞可减轻EAE的严重程度，并有助于中枢神经系统炎症的恢复（4）。Othy等人的报告。（5）揭示了Th17细胞，Treg细胞和APC的时空相互作用及其在EAE的三个不同阶段的迁移。它还显示了Treg细胞如何调节脊髓Th17细胞中的Ca ²⁺信号。