THE PI-LINKED RECEPTOR FCRIII IS RELEASED ON STIMULATION OF NEUTROPHILS
THE PI-LINKED RECEPTOR FCRIII IS RELEASED ON STIMULATION OF NEUTROPHILS
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DOI：
10.1038/333667a0
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发表时间：
1988-06-16
期刊：
影响因子：
64.8
通讯作者：
TETTEROO, PAT
中科院分区：
文献类型：
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作者：
HUIZINGA, TWJ;VANDERSCHOOT, CE;TETTEROO, PAT
人吞噬细胞表达免疫球蛋白G恒定区（Fc）的受体。中性粒细胞携带Fc受体II（FcRII; CDw 32）和FcRIII（CD 16）1- 3，两者均结合含IgG的免疫复合物，导致复合物的吞噬作用和嗜中性粒细胞的激活4，5。我们发现，阵发性睡眠性血红蛋白尿症（PNH）患者的中性粒细胞上FcRIII的水平只有正常水平的10%左右，而FcRII的表达不受影响。我们表明，FcRIII是一种磷脂酰肌醇（PI）锚定蛋白在中性粒细胞。PNH患者细胞中FcRIII表达的分析表明，FcRIII在单核细胞中不是Pi-连接的，已知PNH患者缺乏Pi-连接的蛋白。我们发现，从PNH患者的中性粒细胞中的FcRIII的合成似乎正常，表明缺陷在于PI连接。中性粒细胞上受体的这种脂质连接表明其释放对其功能可能是重要的，并且确实在炎性细菌肽（f-Met-Leu-Phe）刺激中性粒细胞时观察到FcRIII释放，表明FcRIII脱落在炎性反应中的作用。用IgG包被的乳胶珠激活PNH中性粒细胞似乎正常（尽管二聚体IgG复合物的结合减少），表明FcRII而不是FcRIII参与中性粒细胞刺激。
Human phagocytic cells express receptors for the constant (Fc) region of immunoglobulin G. Neutrophils carry Fc receptor II (FcRII; CDw32) and FcRIII (CD16)1–3which both bind IgG-containing immune complexes, leading to phagocytosis of the complex and activation of the neutrophil4,5. We find that patients with paroxysmal nocturnal haemoglobinuria (PNH) have only about 10% of the normal levels of FcRIII on their neutrophils, whereas the expression of FcRII is unaffected. We show that FcRIII is a phosphatidyl inositol (Pl)-anchored protein in neutrophils. Analysis of FcRIII expression in cells of PNH patients, known to be deficient in Pi-linked proteins, suggests FcRIII is not Pi-linked in monocytes. We find that the synthesis of FcRIII in neutrophils from PNH patients appears normal, indicating that the defect lies in the PI linkage. This lipid linkage of the receptor on neutrophils suggests that its release may be important for its function, and indeed FcRIII release was observed on stimulation of neutrophils by an inflammatory bacterial peptide (f-Met-Leu-Phe), suggesting a role for FcRIII shedding in inflammatory reactions. Activation of the PNH neutrophils with IgG-coated latex beads appeared normal (although binding of dimer IgG complexes was reduced), indicating that FcRII, rather than FcRIII, is involved in neutrophil stimulation.