Modjeski K L, Levy S C, Ture S K, Field D J, Shi G, Ko K, Zhu Q, Morrell C N
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.
Am J Transplant. 2016 May;16(5):1383-93. doi: 10.1111/ajt.13623. Epub 2016 Feb 25.
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.
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。