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霍乱毒素对淋巴细胞和单核吞噬细胞Fc受体活性的影响。

Effects of cholera exotoxin on Fc receptor activity of lymphoid cells and mononuclear phagocytes.

作者信息

Zuckerman S H, Douglas S D

出版信息

Immunology. 1977 Mar;32(3):247-53.

PMID:191391
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1445267/
Abstract

The effect of cholera exotoxin and aminophylline on Fc receptors in a murine lymphoid-cell line and in rabbit pulmonary alveolar macrophages has been investigated. Although both agents elevated intracellular cyclic AMP levels in macrophages and lymphoid cells, the effects on Fc receptor expression were distinct. Cholera toxin at 10 microng/ml reversibly inhibited Fc-receptor activity in the murine lymphoid cell line. In contrast, cholera toxin at 10 microng/ml or 0-01 microng/ml was ineffective in altering pulmonary alveolar macrophage receptor expression. Fc receptor activity on the macrophage was reduced by 20-30 per cent following incubation with aminophylline, (10(-3)M) from 0-6 h. There was no direct correlation between Fc-receptor activity and cyclic AMP levels in the cells studied. The differential susceptibility of these lymphoid and phagocytic cell populations to cholera toxin and also toward aminophylline suggests that there may be fundamental differences in topography on the membrane surface, or in the intracellular regulation of Fc receptors between lymphoid and phagocytic cells.

摘要

已研究了霍乱毒素和氨茶碱对小鼠淋巴细胞系及兔肺泡巨噬细胞中Fc受体的作用。尽管这两种药物均可提高巨噬细胞和淋巴细胞内的环磷酸腺苷(cAMP)水平,但对Fc受体表达的影响却截然不同。10微克/毫升的霍乱毒素可可逆性抑制小鼠淋巴细胞系中的Fc受体活性。相比之下,10微克/毫升或0.01微克/毫升的霍乱毒素对改变肺泡巨噬细胞受体表达无效。巨噬细胞与10⁻³M氨茶碱孵育0至6小时后,其Fc受体活性降低了20%至30%。在所研究的细胞中,Fc受体活性与cAMP水平之间无直接相关性。这些淋巴细胞和吞噬细胞群体对霍乱毒素以及氨茶碱的不同敏感性表明,淋巴细胞和吞噬细胞在膜表面拓扑结构或Fc受体的细胞内调节方面可能存在根本差异。

相似文献

1
Effects of cholera exotoxin on Fc receptor activity of lymphoid cells and mononuclear phagocytes.霍乱毒素对淋巴细胞和单核吞噬细胞Fc受体活性的影响。
Immunology. 1977 Mar;32(3):247-53.
2
Inhibition of Fc receptors on a murine lymphoid cell line by cholera exotoxin.
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引用本文的文献

1
Loss of Fc receptor activity after culture of human monocytes on surface-bound immune complexes. Mediation by cyclic nucleotides.人单核细胞在表面结合免疫复合物上培养后Fc受体活性丧失。环核苷酸的介导作用。
J Exp Med. 1980 Jan 1;151(1):32-44. doi: 10.1084/jem.151.1.32.
2
Pathophysiological effects of Vibrio cholerae and enterotoxigenic Escherichia coli and their exotoxins on eucaryotic cells.霍乱弧菌和产肠毒素大肠杆菌及其外毒素对真核细胞的病理生理作用。
Microbiol Rev. 1978 Sep;42(3):592-613. doi: 10.1128/mr.42.3.592-613.1978.

本文引用的文献

1
The adsorption of antigen by spleen cells previously treated with antiserum in vitro.抗原被体外经抗血清处理过的脾细胞吸附。
Immunology. 1960 Jul;3(3):272-83.
2
Studies on pulmonary alveolar macrophages from the normal rabbit: a technique to procure them in a high state of purity.对正常兔肺泡巨噬细胞的研究:一种获取高纯度肺泡巨噬细胞的技术。
J Immunol. 1961 Feb;86:128-32.
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A receptor for antibody on B lymphocytes. I. Method of detection and functional significance.B淋巴细胞上的抗体受体。I. 检测方法及功能意义。
J Exp Med. 1972 Mar 1;135(3):610-26. doi: 10.1084/jem.135.3.610.
4
Phagocytosis of immune complexes by macrophages. Different roles of the macrophage receptor sites for complement (C3) and for immunoglobulin (IgG).巨噬细胞对免疫复合物的吞噬作用。巨噬细胞补体(C3)受体位点和免疫球蛋白(IgG)受体位点的不同作用。
J Exp Med. 1972 Apr 1;135(4):780-92. doi: 10.1084/jem.135.4.780.
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IgG subclass specificity of human monocyte receptor sites.人类单核细胞受体位点的IgG亚类特异性
Nature. 1971 Feb 5;229(5284):419-20. doi: 10.1038/229419a0.
6
The macrophage receptor for IgG: number and affinity of binding sites.免疫球蛋白G的巨噬细胞受体:结合位点的数量与亲和力
J Immunol. 1973 Jun;110(6):1455-63.
7
Lymphocyte mediated cytotoxicity in vitro. Induction and inhibition by humoral antibody and nature of effector cells.体外淋巴细胞介导的细胞毒性。体液抗体的诱导和抑制作用以及效应细胞的性质。
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8
Human T lymphocyte "E" rosette function. I. A process modulated by intracellular cyclic AMP.人T淋巴细胞“E”花环功能。I. 一个受细胞内环磷酸腺苷调节的过程。
J Exp Med. 1974 Oct 1;140(4):1122-6. doi: 10.1084/jem.140.4.1122.
9
Modulation of polymorphonuclear leukocyte-mediated antibody-dependent cellular cytotoxicity.多形核白细胞介导的抗体依赖性细胞毒性的调节
J Immunol. 1974 Dec;113(6):1793-800.
10
Role of cyclic adenosine 3',5'-monophosphate in lymphocyte mitogenesis.环磷酸腺苷在淋巴细胞有丝分裂中的作用。
J Immunol. 1974 Jul;113(1):151-61.