PD-1 /PD-L1 Adoptive Checkpoint Biosynthesis Separately Are Regulated By Gamma Common Which Regulate PD-1, Globin, and IFN-Gamma

Ashraf Marzouk El Tantawi
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Abstract

PD-1 /PD-L1 is adoptive checkpoint mechanism, where PD-1 is an adopting its PD-L1 ligand activities by presence of specific helical kinase proteins in its compositions: _gamma common chains,_LNK” lymphocyte adaptor protein, _or SH2B adaptor _protein “tyrosine kinases, and _”SOCS” suppressor of cytokine signaling, that specified for controlling PD-1 and PD-L1 bindings activity through temporary resting the PD-L1 and consequently T-cells activities then transform incoming signals to exogenous processes in favor the of proper immune functions, But the permanent inhibition of PD-1 /PD-L1 binding is due to breaking down or inhibition in one or more of the adaptors helical proteins (lymphocyte adaptor protein, or SH2B) with the presence of SOCS” suppressor of cytokine signaling that will increase stability of binding without adopting and without activities, but cells survival can still exist through presence of tyrosine kinases , interferon stimulate kinases ,and gamma common.
PD-1 /PD-L1过继性检查点生物合成分别由调节PD-1,球蛋白和ifn - γ的γ Common调节
PD-1 /PD-L1是过继性检查点机制,其中PD-1是通过在其组成物中存在特定的螺旋激酶蛋白来采用其PD-L1配体的活性:_gamma公共链,_LNK“淋巴细胞接头蛋白,_或SH2B接头蛋白”酪氨酸激酶,以及_“SOCS”细胞因子信号抑制因子,它们通过暂时静止PD-L1来控制PD-1和PD-L1的结合活性,从而使t细胞活性将传入的信号转化为外源性过程,从而有利于适当的免疫功能。但是PD-1 /PD-L1结合的永久性抑制是由于SOCS“细胞因子信号抑制因子”的存在破坏或抑制了一个或多个接头螺旋蛋白(淋巴细胞接头蛋白,或SH2B),这将增加结合的稳定性,而不采用和不具有活性,但细胞存活仍然可以通过酪氨酸激酶,干扰素刺激激酶和γ - common的存在而存在。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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