Chan H T, Kedzierska K, O'Mullane J, Crowe S M, Jaworowski A
AIDS Pathogenesis Research Unit, Macfarlane Burnet Centre for Medical Research, Fairfield, Victoria, Australia.
Immunol Cell Biol. 2001 Oct;79(5):429-35. doi: 10.1046/j.1440-1711.2001.01027.x.
The present study demonstrates that SRBC can be opsonized with untreated human serum such that lysis by active complement components is minimal but sufficient opsonization occurs to permit high rates of complement-mediated phagocytosis. Phagocytosis of SRBC opsonized with 2% whole human serum by human monocyte-derived macrophages was quantified in a colourimetric assay. Ingestion of SRBC was shown to occur solely via complement receptors because no phagocytosis was observed when SRBC were coated with heat- inactivated human serum, phagocytosis was augmented by the phorbol ester, PMA, and phagocytosis was inhibited by a protein kinase C (PKC)-specific inhibitor RO 31-8220. This method was used to demonstrate directly that HIV-1 infection of human monocyte-derived macrophages inhibits complement-mediated phagocytosis and will provide a useful tool for pharmacological investigations on complement-mediated phagocytosis by adherent macrophages.
本研究表明，绵羊红细胞（SRBC）可用未经处理的人血清进行调理，使得活性补体成分的裂解作用最小，但发生了足够的调理作用，以允许补体介导的吞噬作用以高比率发生。在比色测定中对人单核细胞衍生的巨噬细胞吞噬经2%全人血清调理的SRBC的情况进行了定量。结果显示，SRBC的摄取仅通过补体受体发生，因为当SRBC用热灭活的人血清包被时未观察到吞噬作用，佛波酯PMA增强了吞噬作用，而蛋白激酶C（PKC）特异性抑制剂RO 31-8220抑制了吞噬作用。该方法被用于直接证明人单核细胞衍生的巨噬细胞感染HIV-1会抑制补体介导的吞噬作用，并将为对黏附巨噬细胞的补体介导吞噬作用进行药理学研究提供一个有用的工具。
