Leu R W, Hefley S M, Herriott M J
Cell Immunol. 1983 Aug;80(1):31-42. doi: 10.1016/0008-8749(83)90091-6.
Guinea pig macrophage populations previously established to be either responsive or refractory to activation by migration inhibitory factor (MIF) and Lotus fucolectin in the macrophage migration inhibition (MMI) assay were further characterized for their MMI response to diverse effectors as correlated with their Fc and C3b receptor function. MIF-refractory populations were found to be uniformly unresponsive to the complement activators: bacterial lipopolysaccharide, cobra venom factor, zymosan, and immune complex. MIF-responsive macrophages were responsive to the same activators. Fc-mediated binding and phagocytosis of IgG-coated sheep erythrocytes (EA) were markedly depressed in freshly harvested refractory macrophages as compared to responsive cells. Fc phagocytosis by refractory populations increased rapidly during 24-28 hr in vitro culture to levels equal to that of responsive cells which corresponded with an increase in their MMI response to MIF. Refractory macrophages also had decreased C3b receptor function as shown by reduced binding and phagocytosis of EAC or serum-coated zymosan and displayed a greater loss in C3b binding capacity than responsive cells during 48 hr in vitro culture. Trypsinization of responsive macrophages rendered them refractory in their MMI response to the various activators and selectively reversed C3b-dependent binding without effect on Fc binding. The plasmin esterase inhibitors, epsilon-amino-n-caproic acid, tranexamic acid, and L-lysine, previously established to reverse the MMI response to MIF, FBP, and C3 activators were found to inhibit both Fc- and C3-dependent phagocytosis. These results indicate that macrophage populations which are refractory to migration inhibition by MIF and C3 activators also have reduced Fc- and C3b-mediated phagocytic functions as compared to more mature responsive populations.
先前在巨噬细胞迁移抑制（MMI）试验中已确定对迁移抑制因子（MIF）和岩藻糖凝集素激活有反应或无反应的豚鼠巨噬细胞群体，进一步就其对多种效应物的MMI反应进行了表征，并将其与Fc和C3b受体功能相关联。发现对MIF无反应的群体对补体激活剂均无反应：细菌脂多糖、眼镜蛇毒因子、酵母聚糖和免疫复合物。对MIF有反应的巨噬细胞对相同的激活剂有反应。与有反应的细胞相比，新鲜收获的无反应巨噬细胞中IgG包被的绵羊红细胞（EA）的Fc介导结合和吞噬作用明显降低。在体外培养24 - 28小时期间，无反应群体的Fc吞噬作用迅速增加，达到与有反应细胞相当的水平，这与它们对MIF的MMI反应增加相对应。无反应巨噬细胞的C3b受体功能也降低，表现为EAC或血清包被的酵母聚糖的结合和吞噬减少，并且在体外培养48小时期间，其C3b结合能力的丧失比有反应细胞更大。用胰蛋白酶处理有反应的巨噬细胞使其对各种激活剂的MMI反应变得无反应，并选择性地逆转C3b依赖性结合，而对Fc结合无影响。先前已确定能逆转对MIF、FBP和C3激活剂的MMI反应的纤溶酶酯酶抑制剂ε-氨基-n-己酸、氨甲环酸和L-赖氨酸，被发现能抑制Fc和C3依赖性吞噬作用。这些结果表明，与更成熟的有反应群体相比，对MIF和C3激活剂的迁移抑制无反应的巨噬细胞群体的Fc和C3b介导的吞噬功能也降低。
