Recruitment of tyrosine phosphatase HCP by the killer cell inhibitory receptor
Recruitment of tyrosine phosphatase HCP by the killer cell inhibitory receptor
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DOI：
10.1016/s1074-7613(00)80300-3
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发表时间：
1996-01-01
期刊：
影响因子：
32.4
通讯作者：
Long, EO
中科院分区：
文献类型：
--
作者：
Burshtyn, DN;Scharenberg, AM;Long, EO
自然杀伤（NK）细胞和一些细胞毒性T细胞对靶细胞的细胞溶解发生，除非被识别靶细胞上的MHC I类的抑制性受体阻止。人NK细胞表达对HLA-C特异性的p58抑制性受体。我们报告协会的酪氨酸磷酸酶HCP与p58受体在NK细胞。HCP的关联依赖于p58的酪氨酸磷酸化。对应于p58尾部的磷酸酪氨酰肽在体外结合和活化HCP。此外，将失活的突变HCP引入NK细胞系防止了p58介导的靶细胞溶解的抑制。这些数据意味着p58的抑制功能依赖于其酪氨酸磷酸化和HCP的募集和激活。
Cytolysis of target cells by natural killer (NK) cells and by some cytotoxic T cells occurs unless prevented by inhibitory receptors that recognize MHC class I on target cells. Human NK cells express a p58 inhibitory receptor specific for HLA-C. We report association of the tyrosine phosphatase HCP with the p58 receptor in NK cells. HCP association was dependent on tyrosine phosphorylation of p58. Phosphotyrosyl peptides corresponding to the p58 tail bound and activated HCP in vitro. Furthermore, introduction of an inactive mutant HCP into an NK cell line prevented the p58-mediated inhibition of target cell lysis. These data imply that the inhibitory function of p58 is dependent on its tyrosine phosphorylation and on recruitment and activation of HCP.