Studies on effector molecules of innate immunity responsible for cytotoxicity to tumor cells.

A.通过硫苷脂增强CR 3介导的嗜中性粒细胞吞噬作用硫苷脂是L-选择素的配体并触发人嗜中性粒细胞中的细胞内信号。我们首次发现，增强CR 3介导的人中性粒细胞吞噬硫苷脂。FcR介导的吞噬作用不被硫苷脂处理改变我们还观察到，未鉴定的硫苷脂受体存在于人嗜中性粒细胞上并参与吞噬作用的增强。B.在凋亡和恶性细胞上表达的同源补体激活剂。氨基酸序列分析与延伸因子1α完全一致。用抗EF-1抗体去除同源补体激活剂活性。我们发现了一种M161抗原，它在人类恶性肿瘤细胞上表达并诱导同源补体激活。M161 Ag的cDNA序列与发酵支原体基因产物P48高度同源。研究表明，潜伏感染的发酵支原体允许人类细胞产生M161 Ag，M161 Ag是通过其补体激活和精氨酸产生活性的先天性和细胞免疫应答的有效调节剂。

A.Enhancement of CR3-mediated neutrophil phagocytosis by sulfatides.Sulfatides is a ligand for L-selectin and triggers intracellular signals in human neutrophils. We found for the first time the enhancement of CR3-mediated human neutrophil phagocytosis by sulfatides. FcR-mediated phagocytosis was not modified by sulfatides treatment We also observed that unidentified receptor for sulfatides exists on human neutrophils and participates in the enhancement of phagocytosis.B.Homologous complement activators expressed on apoptotic and malignant cells.a ; Apoptotic as well as native T cells were found to contain a homologous complement activator of 50 kDa. Amino acid seqenece analysis was identical to those of elongation factor 1α. The homologous complement activator activity was removed with anti-EF-1α.b. We found a M161Ag, which is expressed on human malignant cells and induces homologous complement activation. cDNA of M161Ag revealed that it is highly homologous to P48, mycoplasma fermentans gene product. It was revealed that latently infected M.fermentans allows human cells to produce M161Ag, which is a potent modulator of innate and cellular immune responses via its complement activating and cytokine-producing activity.