COMPLEMENT RECEPTORS--REGULATION OF EXPRESSION AND CELL BIOLOGY

人类吞噬细胞至少有两类受体介导 吞噬浑浊的颗粒。而Fc受体则构成 补体的介导性吞噬、功能和膜表达 受体处于监管控制之下。已经取得了相当大的进展 去年在理解涉及控制的机制方面取得的进展 这些受体的质膜表达和功能。 我们首先展示了不同的细胞激活剂诱导 补体受体。存在于细胞内的受体潜伏池 补体受体与一类补体受体的细胞内定位 补体受体被阐明。受体的上调也被注意到。 依赖于钙动员。受体的调节 表达本身并不能使细胞介导吞噬作用。 我们还发现了两种可以改变吞噬细胞功能的蛋白质 补体受体。我们研究了其中一种蛋白质的作用， 纤维连接蛋白和佛波酯与补体受体的行为 在中性粒细胞中。佛波醇酯但不能诱导纤维连接蛋白 细胞骨架和温度对CR1配体非依赖性内化的影响 依附的机械主义。这些药物还干扰了CR1的关联 用细胞骨架。合成的二酰甘油也能诱导受体 内部化。佛波醇酯和合成的二酰甘油都能增强 甚至通过质膜表达的CR1的吞噬作用也减少了。 我们还研究了钙在这些过程中的作用。 我们认为CR1的生理激活可能通过 多聚磷酸肌醇通过蛋白激酶C的激活抑制代谢 和钙动员。理解和理解规则的功能 从细胞的角度来看，补体受体是非常重要的 生物学以及疾病的病因学。

Human phagocytes have at least two classes of receptors that mediate phagocytosis of opsonized particles. While Fc receptors constitutively mediated phagocytosis, the function and membrane expresion of complement receptors are under regulatory control. Considerable progress has been made in the last year in understanding the mechanisms involved in control of plasma membrane expression and function fo these receptors. We first showed that a variety of cell activators induce upregulation of complement receptors. Intracellular latent pools of receptors exist for complement receptors and the intracellular location of one class of complement receptors was elucidate. Receptor upregulation was also noted to be dependent upon calcium mobilization. Regulation of receptor expression per se did not enable cells to mediate phagocytosis. We also found two proteins that modify the phagocytic function of complement receptors. We studied the effect of one of these proteins, fibronectin as well as phorbol esters the behavior of complement receptors in neutrophils. Phorbol esters but not fibronectin induce ligand-independent internalization of CR1 by a cytoskeletal and temperature dependent mefchanism. These agents also perturbate the association of CR1 with cytoskeleton. Synthetic diocylglycerol also induce receptor internalization. Both phorbol esters and synthetic diacylglycerols augment phagocytosis even through plasma membrane expression of CR1 is decreased. We also studied the role of calcium in these processes. We propose that the physiologic activation of CR1 may occur via polyphosphoinositied metabolism thorugh the avtivation of protein kinase C and calcium mobilization. Understanding the regulation of function of complement receptors is of importance both from the point of view of cell biology as well as disease pathogensis.