The expression of TCR function depend on the gene rearrangement during ontogeny in nor-mal t cell.
细胞抗原受体(TCR)功能的表达有赖于该基因在正常T淋巴细胞发育过程中的重排。
T cell receptor (TCR)gene rearrangement is an important event in T cell ontogeny that enables T cells to specifically recognise antigens, and any dysregulation in this process may result in diseases.
细胞在成熟过程中通过T细胞表面受体基因重排，从而具有特异性识别抗原的能力，在这一过程中的任何失调都会导致疾病。
Activation of this process in immature T cell by the bindng of the TCR CD3 to self antigens may therefor be the mechanism which produces clonal deletion and consequently self tolerance.
未成熟T细胞通过TCR-CD3 复合物与自身抗原接合激活上述过程可能与克隆清除的形成机制及自我耐受有关。
The first signal is the binding of antigen with TCR on T cells. The second signal is the binding of co-stimulate on the APC with their receptors presenting on T and B lymphocytes.
第一信号为抗原与T细胞受体TCR的结合，第二信号为抗原递呈细胞上的协同刺激分子与T、B淋巴细胞上的受体结合。
Objective To investigate the type and the limitary shared of T-cell receptor(TCR) genes in tumor-infiltrating lymphocytes(TIL) of glioma specimens obtained.
目的 检测人脑胶质瘤中肿瘤浸润淋巴细胞 （TIL）是否存在抗原受体基因的限制性取用及其类型 ，探讨其免疫学和临床意义。
CD47 induces costimulatory signals on activation of T cell, T cell apoptosis and T cell anergy and enhances the efficiency of TCR signaling;
CD4 7是T细胞活化的共刺激因子，活化T细胞凋亡过程，诱导T细胞无反应性，加强TCR信号传导的效率；
CD47 induces costimulatory signals on activation of T cell, T cell apoptosis and T cell anergy and enhances the efficiency of TCR signaling;
CD4 7是T细胞活化的共刺激因子，活化T细胞凋亡过程，诱导T细胞无反应性，加强TCR信号传导的效率；
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