Takizawa F, Tsuji S, Nagasawa S
Faculty of Pharmaceutical Sciences, Hokkaido University, Sapporo, Japan.
FEBS Lett. 1996 Nov 18;397(2-3):269-72. doi: 10.1016/s0014-5793(96)01197-0.
Apoptotic cells activate homologous complement and are opsonized with iC3b. We assessed the effect of iC3b opsonization upon phagocytosis of apoptotic Jurkat cells by macrophages, which were differentiated from THP-1 cells by treatment with retinoic acid. Macrophage phagocytosis of apoptotic Jurkat cells was enhanced upon incubation of the apoptotic cells with normal human serum. The enhanced macrophage phagocytosis of normal serum-treated apoptotic cells was decreased by anti-human C3 F(ab')2 and anti-CR3 and anti-CR4 mAbs to the level of phagocytosis of those treated with complement-blocked serum. These results suggest that interaction between iC3b on apoptotic cells and complement receptor type 3 (CR3) and/or complement receptor type 4 (CR4) on macrophages could play an important role for the clearance of apoptotic cells by macrophages in vivo.
凋亡细胞激活同源补体并被iC3b调理。我们评估了iC3b调理对巨噬细胞吞噬凋亡Jurkat细胞的影响,这些巨噬细胞是通过用视黄酸处理THP-1细胞而分化得到的。凋亡Jurkat细胞与正常人血清孵育后,巨噬细胞对其吞噬作用增强。抗人C3 F(ab')2、抗CR3和抗CR4单克隆抗体可将正常血清处理的凋亡细胞增强的巨噬细胞吞噬作用降低至补体阻断血清处理细胞的吞噬水平。这些结果表明,凋亡细胞上的iC3b与巨噬细胞上的补体受体3(CR3)和/或补体受体4(CR4)之间的相互作用可能在体内巨噬细胞清除凋亡细胞中起重要作用。