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谷氨酸受体相互作用蛋白1调节CD4(+) CTLA-4表达及移植排斥反应。

Glutamate Receptor Interacting Protein 1 Regulates CD4(+) CTLA-4 Expression and Transplant Rejection.

作者信息

Modjeski K L, Levy S C, Ture S K, Field D J, Shi G, Ko K, Zhu Q, Morrell C N

机构信息

Aab Cardiovascular Research Institute, University of Rochester School of Medicine and Dentistry, Rochester, NY.

Department of Pharmacology and Physiology, University of Rochester School of Medicine and Dentistry, Rochester, NY.

出版信息

Am J Transplant. 2016 May;16(5):1383-93. doi: 10.1111/ajt.13623. Epub 2016 Feb 25.

Abstract

PDZ domains are common 80- to 90-amino-acid regions named after the first three proteins discovered to share these domains: postsynaptic density 95, discs large, and zonula occludens. PDZ domain-containing proteins typically interact with the C-terminus of membrane receptors. Glutamate receptor interacting protein 1 (GRIP1), a seven-PDZ domain protein scaffold, regulates glutamate receptor surface expression and trafficking in neurons. We have found that human and mouse T cells also express GRIP1. T cell-specific GRIP1(-/-) mice >11 weeks old had prolonged cardiac allograft survival. Compared with wild-type T cells, in vitro stimulated GRIP1(-/-) T cells had decreased expression of activation markers and increased apoptotic surface marker expression. Surface expression of the strong T cell inhibitory molecule cytotoxic T lymphocyte antigen-4 (CTLA-4) was increased on GRIP1(-/-) T cells from mice >11 weeks old. CTLA-4 increases with T cell stimulation and its surface expression on GRIP1(-/-) T cells remained high after stimulation was removed, indicating a possible internalization defect in GRIP1-deficient T cells. CTLA-4-blocking antibody treatment following heart transplantation led to complete rejection in T cell GRIP1(-/-) mice, indicating that increased CTLA-4 surface expression contributed to the extended graft survival. Our data indicate that GRIP1 regulates T cell activation by regulating CTLA-4 surface expression.

摘要

PDZ结构域是常见的由80至90个氨基酸组成的区域,其命名源于最初发现的三种共享这些结构域的蛋白质:突触后致密蛋白95、盘状大蛋白和紧密连接蛋白。含PDZ结构域的蛋白质通常与膜受体的C末端相互作用。谷氨酸受体相互作用蛋白1(GRIP1)是一种含有七个PDZ结构域的蛋白质支架,可调节谷氨酸受体在神经元中的表面表达和运输。我们发现人和小鼠的T细胞也表达GRIP1。11周龄以上的T细胞特异性GRIP1基因敲除(-/-)小鼠的心脏移植存活时间延长。与野生型T细胞相比,体外刺激的GRIP1(-/-)T细胞的激活标志物表达降低,凋亡表面标志物表达增加。在11周龄以上小鼠的GRIP1(-/-)T细胞上,强T细胞抑制分子细胞毒性T淋巴细胞抗原4(CTLA-4)的表面表达增加。CTLA-4随着T细胞刺激而增加,在去除刺激后,其在GRIP1(-/-)T细胞上的表面表达仍保持较高水平,这表明GRIP1缺陷型T细胞可能存在内化缺陷。心脏移植后用CTLA-4阻断抗体治疗导致T细胞GRIP1(-/-)小鼠完全排斥,这表明CTLA-4表面表达增加有助于延长移植物存活时间。我们的数据表明,GRIP1通过调节CTLA-4表面表达来调节T细胞激活。

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4
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5
Tyrosine 201 of the cytoplasmic tail of CTLA-4 critically affects T regulatory cell suppressive function.
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6
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7
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8
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