Yefenof E, Asjö B, Klein E
Lautenberg Center for General & Tumor Immunology, Hebrew University-Hadassah Medical School, Jerusalem, Israel.
Int Immunol. 1991 Apr;3(4):395-401. doi: 10.1093/intimm/3.4.395.
HIV infected T and monocytic cell lines could activate and fix C3 fragments when incubated in human serum under conditions allowing for activation of the alternative complement pathway. Normal T lymphocytes incubated with HIV could also activate and fix C3. This activity was, at least in part, the property of the virus itself since cell-free HIV could efficiently activate C3. The C3 activating HIV infected cells were resistant to complement-mediated lysis, even after prolonged incubation periods. However, their sensitivity to cell-mediated natural killing increased, presumably due to their interaction with complement receptor bearing NK lymphocytes. The results suggest that the alternative complement pathway may contribute to the depletion of CD4+ T lymphocytes during HIV infection in vivo.
在允许替代补体途径激活的条件下，当在人血清中孵育时，感染HIV的T细胞系和单核细胞系能够激活并固定C3片段。与HIV一起孵育的正常T淋巴细胞也能激活并固定C3。这种活性至少部分是病毒本身的特性，因为无细胞HIV能够有效地激活C3。激活C3的HIV感染细胞对补体介导的裂解具有抗性，即使经过长时间孵育也是如此。然而，它们对细胞介导的自然杀伤的敏感性增加，推测是由于它们与带有补体受体的NK淋巴细胞相互作用。结果表明，替代补体途径可能在体内HIV感染期间导致CD4 + T淋巴细胞的耗竭。
