Neuroinflammation: Extinguishing a blaze of T cells.

Neuroinflammation: Extinguishing a blaze of T cells.
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DOI:
10.1111/imr.13122
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发表时间:
2022-10
影响因子:
8.7
通讯作者:
--
中科院分区:
医学1区
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--
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炎症是一个动态改变周围微环境的生物学过程,包括参与的免疫细胞。中枢神经系统(CNS)是一个被专门屏障包围并具有免疫豁免特性的受保护器官,它严格调节免疫反应。然而,在神经炎症条件下,病原性免疫可以破坏CNS结构和功能。特别是T细胞在促进和限制神经炎症反应中起着关键作用,而炎症的CNS微环境可以影响和重塑T细胞的功能和身份。尽管如此,CNS内异常T细胞反应的收缩仍不清楚。使用自身免疫作为模型,在这里,我们解决的贡献CD4辅助性T(Th)细胞亚群在促进神经病理和疾病。为了解决拮抗神经炎症的机制,我们专注于调节性T细胞(TCFs)对免疫反应的控制,并描述了在炎症挑战下保持其身份的抵消过程。最后,考虑到局部微环境对免疫调节的影响,我们讨论了CNS内在信号如何重塑T细胞功能以减轻异常的免疫T细胞反应。
Inflammation is a biological process that dynamically alters the surrounding microenvironment, including participating immune cells. As a well-protected organ surrounded by specialized barriers and with immune privilege properties, the central nervous system (CNS) tightly regulates immune responses. Yet in neuroinflammatory conditions, pathogenic immunity can disrupt CNS structure and function. T cells in particular play a key role in promoting and restricting neuroinflammatory responses, while the inflamed CNS microenvironment can influence and reshape T cell function and identity. Still, the contraction of aberrant T cell responses within the CNS is not well understood. Using autoimmunity as a model, here we address the contribution of CD4 T helper (Th) cell subsets in promoting neuropathology and disease. To address the mechanisms antagonizing neuroinflammation, we focus on the control of the immune response by regulatory T cells (Tregs) and describe the counteracting processes that preserve their identity under inflammatory challenges. Finally, given the influence of the local microenvironment on immune regulation, we address how CNS-intrinsic signals reshape T cell function to mitigate abnormal immune T cell responses.
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