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首页> 外文期刊>Journal of Leukocyte Biology: An Official Publication of the Reticuloendothelial Society >Contribution of mannose receptor to signal transduction in Fc gamma receptor-mediated phagocytosis of mouse peritoneal macrophages induced by liposomes.
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Contribution of mannose receptor to signal transduction in Fc gamma receptor-mediated phagocytosis of mouse peritoneal macrophages induced by liposomes.

机译:甘露糖受体对Fcγ受体介导的脂质体诱导的小鼠腹膜巨噬细胞吞噬作用中信号转导的贡献。

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The contribution of mannose receptors on the cell surface of mouse peritoneal macrophages to the process of liposome-induced phagocytosis of immunoglobulin G-opsonized sheep red blood cells (SRBCs) through Fc gamma receptor has been investigated. Fc gamma receptor-mediated phagocytosis of opsonized SRBCs was activated by modified alpha 2-macroglobulin, which was produced in the incubation mixture of alpha 2-macroglobulin and liposome-treated splenic B cells. The phagocytosis was specifically inhibited by the addition of D-mannose, and the inhibition was dependent on the D-mannose concentration. The binding of modified alpha 2-macroglobulin to macrophages was also reduced by the addition of D-mannose. The activation effect of modified alpha 2-macroglobulin was not inhibited when in the presence of alpha 2-macroglobulin-trypsin and -methylamine complexes. In the presence of cycloheximide, activated phagocytosis was reduced to the control level. By Scatchard plot analysis of IgG binding studies, the number of Fc gamma receptors of a macrophage had been increased to 4.6-fold that of a control macrophage by treatment with modified alpha 2-macroglobulin. These findings suggest that macrophage mannose receptors are involved in activating the process of Fc gamma receptor-mediated phagocytosis of opsonized SRBCs induced by modified alpha 2-macroglobulin. Lectins may participate in a signal transduction in macrophage activation by liposomes.
机译:已经研究了小鼠腹膜巨噬细胞表面甘露糖受体对脂质体通过Fcγ受体诱导的免疫球蛋白G调理绵羊红细胞(SRBCs)吞噬过程的贡献。 Fcγ受体介导的调理SRBC吞噬作用被修饰的α2-巨球蛋白激活,该α2-巨球蛋白是在α2-巨球蛋白和脂质体处理的脾B细胞的孵育混合物中产生的。通过添加D-甘露糖可特异性抑制吞噬作用,并且该抑制作用取决于D-甘露糖浓度。通过添加D-甘露糖也减少了修饰的α2-巨球蛋白与巨噬细胞的结合。当存在α2-巨球蛋白-胰蛋白酶和-甲胺复合物时,修饰的α2-巨球蛋白的活化作用不被抑制。在存在环己酰亚胺的情况下,激活的吞噬作用降低至对照水平。通过IgG结合研究的Scatchard图分析,通过用修饰的α2-巨球蛋白处理,巨噬细胞的Fcγ受体的数目已经增加至对照巨噬细胞的4.6倍。这些发现表明巨噬细胞甘露糖受体参与激活由修饰的α2-巨球蛋白诱导的调理SRBC的Fcγ受体介导的吞噬作用的过程。凝集素可参与脂质体在巨噬细胞激活中的信号转导。

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