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Nat Immunol. 2022 May;23(5):743-756. doi: 10.1038/s41590-022-01170-w. Epub 2022 Apr 18.
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J Autoimmun. 2022 May;129:102816. doi: 10.1016/j.jaut.2022.102816. Epub 2022 Apr 5.
3
Hedgehog Signalling Modulates Immune Response and Protects against Experimental Autoimmune Encephalomyelitis.Hedgehog 信号通路调节免疫反应并预防实验性自身免疫性脑脊髓炎。
Int J Mol Sci. 2022 Mar 15;23(6):3171. doi: 10.3390/ijms23063171.
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Novel Th17 Lymphocyte Populations, Th17.1 and PD1+Th17, are Increased in Takayasu Arteritis, and Both Th17 and Th17.1 Sub-Populations Associate with Active Disease.新型Th17淋巴细胞亚群,即Th17.1和PD1+Th17,在大动脉炎中增多,且Th17和Th17.1亚群均与疾病活动相关。
J Inflamm Res. 2022 Mar 1;15:1521-1541. doi: 10.2147/JIR.S355881. eCollection 2022.
6
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RORγt Promotes Foxp3 Expression by Antagonizing the Effector Program in Colonic Regulatory T Cells.RORγt 通过拮抗结肠调节性 T 细胞中的效应程序促进 Foxp3 表达。
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神经炎症:扑灭 T 细胞之火。

Neuroinflammation: Extinguishing a blaze of T cells.

机构信息

Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.

Center for Research in Transplantation and Translational Immunology, Nantes Université, CHU Nantes, INSERM, UMR 1064, Nantes, France.

出版信息

Immunol Rev. 2022 Oct;311(1):151-176. doi: 10.1111/imr.13122. Epub 2022 Jul 31.

DOI:10.1111/imr.13122
PMID:35909230
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9489683/
Abstract

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.

摘要

炎症是一种动态改变周围微环境的生物学过程,包括参与免疫细胞。作为一个被专门的屏障所保护的器官,具有免疫特权特性,中枢神经系统(CNS)严格调节免疫反应。然而,在神经炎症情况下,致病性免疫可能会破坏中枢神经系统的结构和功能。T 细胞在促进和限制神经炎症反应中起着关键作用,而炎症中枢神经系统微环境可以影响和重塑 T 细胞的功能和特性。然而,中枢神经系统内异常 T 细胞反应的收缩还不是很清楚。我们利用自身免疫作为模型,在这里探讨 CD4 辅助性 T 细胞(Th)亚群在促进神经病理学和疾病中的作用。为了研究对抗神经炎症的机制,我们专注于调节性 T 细胞(Tregs)对免疫反应的控制,并描述在炎症挑战下维持其特性的拮抗过程。最后,鉴于局部微环境对免疫调节的影响,我们探讨了中枢神经系统内在信号如何重塑 T 细胞功能,以减轻异常免疫 T 细胞反应。