TIGIT刺激通过抑制Th17细胞浸润抑制自身免疫性葡萄膜炎

IF 3.6 3区 医学 Q3 CELL BIOLOGY
Kayleigh Peters, Trisha McDonald, Fauziyya Muhammad, Adrien Brady, John Dostal, Darren J Lee
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引用次数: 0

摘要

T细胞免疫球蛋白和ITIM结构域(TIGIT)是一种免疫检查点分子,可抑制T细胞活化并促进免疫抑制环境,从而抑制自身免疫性疾病。然而,TIGIT 激动剂作为眼部自身免疫性疾病治疗的影响尚未得到研究。我们研究了TIGIT在Th17和Treg细胞上的表达、TIGIT对实验性自身免疫性葡萄膜炎(EAU)和Th17细胞的作用以及TIGIT刺激后Treg生成的影响。在临床症状出现时刺激TIGIT可减轻葡萄膜炎的严重程度,并抑制Th17细胞向眼内的浸润。此外,用TIGIT激动剂治疗的小鼠产生的Tregs能够抑制受体小鼠的EAU。该报告表明,在发病初期刺激 TIGIT 可抑制症状并诱导调节性免疫,从而提供对葡萄膜炎的抵抗力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
TIGIT stimulation suppresses autoimmune uveitis by inhibiting Th17 cell infiltration.

T cell immunoglobulin and ITIM domain (TIGIT) is an immune checkpoint molecule that suppresses T cell activation and promotes an immunosuppressive environment to suppress autoimmune diseases. However, the impact of a TIGIT agonist as a treatment for ocular autoimmune disease has not been investigated. We examined TIGIT expression on T helper 17 (Th17) and regulatory T cells (Tregs), the role of TIGIT on experimental autoimmune uveitis and Th17 cells, and the impact of Treg generation following TIGIT stimulation. TIGIT stimulation at the onset of clinical symptoms reduced the severity of uveitis and suppressed infiltration of Th17 cells into the eye. Further, Tregs from mice treated with the TIGIT agonist were capable of suppressing experimental autoimmune uveitis in recipient mice. This report demonstrates that stimulation of TIGIT at onset of disease suppresses symptoms and allows for induction of regulatory immunity that provides resistance to uveitis.

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来源期刊
Journal of Leukocyte Biology
Journal of Leukocyte Biology 医学-免疫学
CiteScore
11.50
自引率
0.00%
发文量
358
审稿时长
2 months
期刊介绍: JLB is a peer-reviewed, academic journal published by the Society for Leukocyte Biology for its members and the community of immunobiologists. The journal publishes papers devoted to the exploration of the cellular and molecular biology of granulocytes, mononuclear phagocytes, lymphocytes, NK cells, and other cells involved in host physiology and defense/resistance against disease. Since all cells in the body can directly or indirectly contribute to the maintenance of the integrity of the organism and restoration of homeostasis through repair, JLB also considers articles involving epithelial, endothelial, fibroblastic, neural, and other somatic cell types participating in host defense. Studies covering pathophysiology, cell development, differentiation and trafficking; fundamental, translational and clinical immunology, inflammation, extracellular mediators and effector molecules; receptors, signal transduction and genes are considered relevant. Research articles and reviews that provide a novel understanding in any of these fields are given priority as well as technical advances related to leukocyte research methods.
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