Alternative complement pathway activation by CD4+ T cells of HIV infected individuals: a possible role in AIDS pathogenesis.
Alternative complement pathway activation by CD4+ T cells of HIV infected individuals: a possible role in AIDS pathogenesis.
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HIV 感染者 CD4 T 细胞激活替代补体途径：在 AIDS 发病机制中的可能作用。
DOI：
10.1093/intimm/6.9.1361
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发表时间：
1994
影响因子：
4.4
通讯作者：
E. Klein
中科院分区：
文献类型：
--
作者：
E. Yefenof;T. Magyarlaki;É. Fenyő;B. Wahren;E. Klein
在HIV感染期间CD4+ T细胞被清除的机制知之甚少。我们先前已经表明，HIV感染的细胞系通过替代补体途径（ACP）激活和固定C3。在本研究中，我们研究了40个HIV阳性个体的血液淋巴细胞固定C3的能力。大部分的CD4+ T细胞与抗gp120抗体反应。这些细胞在体内也携带C3片段，并且如果在体外暴露于人血清，则可以进一步固定C3。C3通过ACP激活。在某些情况下，在允许ACP活化的条件下将淋巴细胞暴露于人血清导致CD4+ T细胞的部分消除。结果表明，补体激活和固定的CD4+ T细胞调理与HIV颗粒或gp120可能有助于他们的选择性破坏。
The mechanisms by which CD4+ T cells are eliminated during HIV infection are poorly understood. We have previously shown that HIV infected cell lines activate and fix C3 via the alternative complement pathway (ACP). In the present study we examined the ability of blood lymphocytes from 40 HIV+ individuals to fix C3. A large fraction of the CD4+ T cells reacted with anti-gp120 antibodies. These cells also carried C3 fragments in vivo and could further fix C3 if exposed to human serum in vitro. C3 activation occurred via the ACP. In some cases exposure of the lymphocytes to human serum under conditions allowing ACP activation resulted in partial elimination of CD4+ T cells. The results suggest that complement activation and fixation by CD4+ T cells opsonized with HIV particles or gp120 may contribute to their selective destruction.