STUDIES ON THE BIOLOGICAL FUNCTIONS OF THE COMPLEMENT SYSTEM

本课题研究了补体系统的生物学功能，主要结果如下：1.凋亡细胞激活自体补体旁路途径。补体激活不发生在同源活细胞上。我们观察到人脐静脉细胞在凋亡过程中激活了人补体旁路途径。凋亡细胞的这种自体补体激活也在人T细胞系AptoticJurkat细胞中观察到。这些发现表明，新的蛋白质应表达在凋亡细胞的表面，以诱导自体补体激活。补体激活导致C3 b衍生物iC 3b调理靶细胞。吞噬细胞如表达C3受体的巨噬细胞，可以吞噬iC 3b包被的细胞。因此，凋亡细胞激活自体补体可能促进吞噬细胞对凋亡细胞的处理.补体受体对Fc受体功能的影响--FcR与CR 3的协同作用我们比较了人中性粒细胞对免疫复合物（IC）和iC 3b-调理衍生物（iC 3b-IC）的吞噬作用。用磷脂酶D抑制剂乙醇处理细胞后，iC 3b-IC的吞噬作用降低到与IC相同的水平。抗FcR Ⅲ B能更有效地抑制IC的吞噬作用，而抗FcR Ⅱ仅能部分抑制iC 3b-IC的吞噬作用。这些结果表明IC和iC 3b-IC吞噬作用中的主要FcR可能不同。

We investigated the biological functions of the complement system, which acts as a host defense for invading cells.The important results obtained bu this project are as follow ;1.Activation of the autologous alternative complement pathway by apoptotic cells. Complement activation does not occur on homologous live cells. We observed the activation of alternative human complement pathway by human umbilical vein cells, when these cells died of apoptotic process. This autologous complement activation by apoptotic cells was also observed with apoptoticJurkat cells, a human T cell line. these findings suggest that novel proteins should be expressed at the surface of apoptotic cell to induce autologouscomplement activation. Complement activation results in the opsonization oftarget cells with C3b derivative, iC3b. Phagocytes sugh as macrophages express C3 receptor and can phagocytose iC3b-coated cells. So, it appears likelythat activation of the autologous complement by apoptotic cells may promote the processing of apoptotic cell by phagocytes.2. The effect of complement receptor upon the functions of Fc receptors--Synergistic function between FcR and CR3. We compared the phagocytosis of immune complexes (IC) and iC3b-opsonized derivatives (iC3b-IC) by human neutrophils. The phagocytosis of iC3b-IC was greater than that of IC.The enhanced phagocytosis of iC3b-IC was decreased to the same level to that of IC upon treatment of cells with ethanol, aninhibitor for phospholipase D.The IC phagocytosis was inhibited more effectively by anti-FcR lllB,whereas the iC3b-lC phagocytosis was partly inhibited only by anti-FcRll . These results in dicate that the main FcR might differin IC and iC3b-IC phagocytosis.