Jarvis J N, Taylor H, Long P M, Gutta P V, Pousak T, Fine N
Department of Pediatrics/Immunology, Wayne State University School of Medicine/Children's Hospital of Michigan 48201, USA.
J Acquir Immune Defic Syndr Hum Retrovirol. 1995 Jul 1;9(3):249-56.
Experimental data have established that HIV-infected lymphocytes activate the complement system. However, because mammalian lymphocytes possess a series of cell-surface complement regulators that inhibit amplification on autologous cells, complement-mediated destruction of host cells is usually inhibited. These studies were performed to examine whether alterations in the cell-surface complement regulatory proteins decay-accelerating factor (DAF, CD55) and membrane cofactor protein (MCP, CD46) may occur during HIV infection in vitro or in vivo. The physiologic significance of these alterations were assessed by radiolabeled chromium release experiments. We show that MCP fluorescent intensity is significantly lessened in HIV-infected children and that DAF intensity is similarly lessened in infected children with advanced disease. These findings could be duplicated with HIV infection of peripheral blood mononuclear cells in vitro.
实验数据已证实,感染HIV的淋巴细胞会激活补体系统。然而,由于哺乳动物淋巴细胞拥有一系列细胞表面补体调节因子,可抑制自身细胞上的补体扩增,因此补体介导的宿主细胞破坏通常受到抑制。开展这些研究是为了检测在体外或体内的HIV感染过程中,细胞表面补体调节蛋白衰变加速因子(DAF,CD55)和膜辅助蛋白(MCP,CD46)是否会发生改变。通过放射性标记的铬释放实验评估了这些改变的生理意义。我们发现,感染HIV的儿童体内MCP荧光强度显著降低,而在病情严重的感染儿童中DAF强度也有类似程度的降低。这些发现可在体外利用外周血单核细胞进行HIV感染时重现。