STUDIES ON THE BIOLOGICAL FUNCTIONS OF THE COMPLEMENT SYSTEM

我们研究了作为入侵细胞宿主防御的补体系统的生物学功能。通过本项目获得的重要结果如下：1.通过凋亡的细胞激活自体替代补体途径。补体激活不会发生在同源活细胞上。我们观察到当人脐静脉细胞死亡时，这些细胞激活了人类补体替代途径。这种由凋亡细胞激活的自体补体也在人类T细胞系Jurkat细胞中观察到。这些发现表明，新的蛋白质应该表达在凋亡细胞的表面，以诱导自体补体激活。补体激活导致靶细胞与C3b衍生物iC3b的调理。吞噬细胞作为巨噬细胞表达C3受体，并能吞噬包被C3b的细胞。因此，似乎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CR3的协同作用我们比较了人中性粒细胞对免疫复合体(IC)和IC3b调理衍生物(IC3b-IC)的吞噬作用。经磷脂酶D抑制剂乙醇处理后，iC3b-IC的吞噬功能增强程度与IC相当。抗FCR111B抗体对IC吞噬功能的抑制作用更强，而抗FcR11抗体仅部分抑制IC3b-LC细胞的吞噬功能。这些结果表明，主要的FCR可能不同于IC和IC3b-IC的吞噬作用。

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.