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Fcμ受体介导的驻留和激发腹膜巨噬细胞功能的调节

Regulation of Fc mu receptor-mediated functions of resident and provoked peritoneal macrophages.

作者信息

Medgyesi G A, Fóris G, Füst G, Bazin H

出版信息

Immunobiology. 1984 Oct;167(4):293-300. doi: 10.1016/s0171-2985(84)80001-7.

DOI:10.1016/s0171-2985(84)80001-7
PMID:6595215
Abstract

Modifying and/or regulating effects on Fc mu receptor (R) mediated phagocytic and ADCC activity of both resident (r) and provoked (p) peritoneal macrophages (PM) was studied applying drugs affecting the cytoskeleton and cation transport. In addition, the effects of exogenous PGE2 and cyclic nucleotides were also examined. Fc mu-receptors appear to be functionally less significant in provoked PMs than in resident ones since both Fc mu-receptor mediated phagocytosis and ADCC were lower in the formers. The cytoskeletal system is important in the regulation of both Fc mu-receptor-mediated functions. Phagocytosis through Fc mu-receptor is decreased by Cytochalasin B and by Vinblastine treatment, whereas ADCC is enhanced by Cytochalasin B. Extracellular PGE2 and cAMP induced a higher phagocytic activity and suppressed ADCC, whereas cGMP displayed an opposite effect. The sensitivity of Fc mu R-mediated activities to ionophoric and to cytoskeleton-damaging drugs was lower in provoked than in resident PMs. In addition, the regulatory role of PGE2 and of cyclic nucleotides on the same activities was less marked on provoked PMs. In contrast, ouabain inhibits Fc mu R-dependent antigen incorporation and ADCC on provoked PM monolayers only. These findings suggest differing regulatory mechanisms for Fc mu R-mediated functions in provoked PMs as compared with resident ones.

摘要

应用影响细胞骨架和阳离子转运的药物,研究了对常驻(r)和激发(p)腹膜巨噬细胞(PM)的Fcμ受体(R)介导的吞噬作用和抗体依赖的细胞介导的细胞毒性(ADCC)活性的调节和/或调控作用。此外,还研究了外源性前列腺素E2(PGE2)和环核苷酸的作用。Fcμ受体在激发的PM中的功能重要性似乎低于常驻PM,因为前者的Fcμ受体介导的吞噬作用和ADCC均较低。细胞骨架系统在调节Fcμ受体介导的功能中起重要作用。用细胞松弛素B和长春碱处理可降低通过Fcμ受体的吞噬作用,而细胞松弛素B可增强ADCC。细胞外PGE2和环磷酸腺苷(cAMP)诱导更高的吞噬活性并抑制ADCC,而环磷酸鸟苷(cGMP)则表现出相反的作用。激发的PM对离子载体和细胞骨架损伤药物的FcμR介导的活性敏感性低于常驻PM。此外,PGE2和环核苷酸对激发的PM的相同活性的调节作用较小。相反,哇巴因仅抑制激发的PM单层上FcμR依赖性抗原掺入和ADCC。这些发现表明,与常驻PM相比,激发的PM中FcμR介导的功能具有不同的调节机制。

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