Spear G T, Landay A L, Sullivan B L, Dittel B, Lint T F
Department of Immunology/Microbiology, Rush-Presbyterian-St. Luke's Medical Center, Chicago, IL 60612.
J Immunol. 1990 Feb 15;144(4):1490-6.
Cells were infected with HIV-1 and tested for C activation using a flow cytometric assay for bound C3 fragments. HIV-infected H9 cells bound increased levels of C3 using normal human serum as a C source only after cells were first incubated with serum containing anti-HIV antibody. Uninfected H9 cells or infected cells incubated with HIV-antibody negative sera did not bind C3. Although C3 bound quickly and was maximal within 10 min, modulation of bound C3 was slow with about 50% loss after 4 h. C3 binding required specific anti-HIV antibody, was blocked by EGTA, and did not occur in C2-deficient serum suggesting that binding was via the classical pathway. The HTLV-1-infected MT-4 cell line also bound high levels of C3 after coinfection with HIV. C3 binding in HIV-infected MT4 cells was also mediated via the classical pathway because it was not observed in Mg-EGTA chelated or C2-deficient sera. However, this classical pathway activation appeared to be antibody independent because it was also detected in HIV-antibody negative serum and a-gamma-globulinemic serum. This indicates that coinfection with HTLV-1 and HIV-1 can produce novel C activating conditions. No cytotoxic effect of human C for antibody-treated HIV-infected cells was observed in a chromium release assay. However, rabbit C was cytotoxic for HIV-infected cells in the absence of anti-HIV antibodies. Our results suggest that C can be activated in vivo by infected cells via specific anti-HIV antibody. The resultant C3 deposition on infected cells could have profound effects on interaction with CR-bearing cells.
细胞用HIV-1感染，并使用针对结合的C3片段的流式细胞术检测补体（C）激活情况。仅在细胞先用含抗HIV抗体的血清孵育后，以正常人血清作为补体来源时，HIV感染的H9细胞结合的C3水平才会增加。未感染的H9细胞或用HIV抗体阴性血清孵育的感染细胞不结合C3。尽管C3结合迅速且在10分钟内达到最大值，但结合的C3的调节较慢，4小时后约有50%损失。C3结合需要特异性抗HIV抗体，被乙二醇双四乙酸（EGTA）阻断，且在C2缺陷血清中不发生，这表明结合是通过经典途径进行的。人嗜T淋巴细胞病毒1型（HTLV-1）感染的MT-4细胞系在与HIV共感染后也结合高水平的C3。HIV感染的MT4细胞中的C3结合也通过经典途径介导，因为在镁-EGTA螯合血清或C2缺陷血清中未观察到。然而，这种经典途径激活似乎与抗体无关，因为在HIV抗体阴性血清和无丙种球蛋白血症血清中也检测到了。这表明HTLV-1和HIV-1共感染可产生新的补体激活条件。在铬释放试验中未观察到人补体对抗体处理的HIV感染细胞的细胞毒性作用。然而，在没有抗HIV抗体的情况下，兔补体对HIV感染细胞具有细胞毒性。我们的结果表明，补体可在体内被感染细胞通过特异性抗HIV抗体激活。由此产生的C3在感染细胞上的沉积可能对与携带补体受体（CR）的细胞的相互作用产生深远影响。
