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鞘氨醇-1-磷酸受体 1 在 T 细胞中的信号转导:运输及其他。

Sphingosine-1-phosphate receptor 1 signalling in T cells: trafficking and beyond.

机构信息

Graduate Program in Immunology, Division of Medical Sciences, Harvard Medical School, Boston, MA, USA.

出版信息

Immunology. 2014 Jul;142(3):347-53. doi: 10.1111/imm.12272.

DOI:10.1111/imm.12272
PMID:24597601
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4080950/
Abstract

Sphingosine-1-phosphate (S1P) is a lipid second messenger that signals via five G protein-coupled receptors (S1P1-5 ). S1P receptor (S1PR) signalling is associated with a wide variety of physiological processes including lymphocyte biology, their recirculation and determination of T-cell phenotypes. The effect of FTY720 (Fingolimod, Gilenya™) to regulate lymphocyte egress and to ameliorate paralysis in experimental autoimmune encephalomyelitis, an animal model of multiple sclerosis led to the use of FTY720 as a first-line oral agent for treatment of relapsing-remitting multiple sclerosis. However, a significant body of research suggests that S1P signalling may participate in diverse immune regulatory functions other than lymphocyte trafficking. This review article discusses the current knowledge of S1P signalling in the fate and function of T regulatory, T helper type 17 and memory T cells in health and disease.

摘要

鞘氨醇-1-磷酸(S1P)是一种脂质第二信使,通过五种 G 蛋白偶联受体(S1P1-5)信号传递。S1P 受体(S1PR)信号与多种生理过程相关,包括淋巴细胞生物学、它们的再循环和 T 细胞表型的决定。FTY720(芬戈莫德,Gilenya™)调节淋巴细胞迁出并改善实验性自身免疫性脑脊髓炎(多发性硬化症的动物模型)中的瘫痪的作用,导致 FTY720 被用作治疗复发性缓解型多发性硬化症的一线口服药物。然而,大量研究表明,S1P 信号传递可能参与除淋巴细胞运输以外的多种免疫调节功能。本文讨论了 S1P 信号传递在健康和疾病状态下 T 调节细胞、辅助性 T 细胞 17 型和记忆 T 细胞的命运和功能中的最新知识。

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本文引用的文献

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Transcriptional downregulation of S1pr1 is required for the establishment of resident memory CD8+ T cells.S1pr1 的转录下调是驻留记忆 CD8+T 细胞建立所必需的。
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Defective sphingosine 1-phosphate receptor 1 (S1P1) phosphorylation exacerbates TH17-mediated autoimmune neuroinflammation.缺陷型鞘氨醇 1-磷酸受体 1(S1P1)磷酸化加重 TH17 介导的自身免疫性神经炎症。
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GRK2-dependent S1PR1 desensitization is required for lymphocytes to overcome their attraction to blood.GRK2 依赖性 S1PR1 脱敏对于淋巴细胞克服对血液的吸引力是必需的。
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STAT3-induced S1PR1 expression is crucial for persistent STAT3 activation in tumors.STAT3 诱导的 S1PR1 表达对于肿瘤中持续的 STAT3 激活至关重要。
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