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B7-H1首先是在与B7-1/B7-2的同源性分析中发现的。可在多数外周和造血组织中诱导表达。通过与na ve T细胞上未定受体结合,B7-H1共刺激T细胞增殖并诱导IL-10和IFN-γ生成。B7-H1的共刺激作用对淋巴器官T细胞的成熟和分化有重要作用。相反,通过结合活化T细胞和B细胞上的PD-1受体,B7-H1诱导凋亡和延滞细胞周期而抑制T细胞反应。在癌症、类风湿、HIV感染等疾病中发现B7-H1有负调节作用。对B7-H1路径进行调控有助于自身免疫病及恶性肿瘤的治疗。
B7-H1 was first found in homology analysis with B7-1 / B7-2. Expression can be induced in most peripheral and hematopoietic tissues. B7-H1 co-stimulates T cell proliferation and induces IL-10 and IFN-γ production by binding to undetermined receptors on na ve T cells. Costimulation of B7-H1 plays an important role in the maturation and differentiation of T lymphocytes in lymphoid organs. In contrast, B7-H1 induces apoptosis and delays cell cycle arrest in T-cell responses by binding to PD-1 receptors on activated T cells and B cells. In cancer, rheumatoid, HIV infection and other diseases found that B7-H1 has a negative regulatory role. Regulation of the B7-H1 pathway can help in the treatment of autoimmune diseases and malignancies.