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FcεRII/CD23和L-精氨酸依赖途径在IgE介导的人嗜酸性粒细胞活化中的作用

Involvement of Fc epsilon RII/CD23 and L-arginine dependent pathway in IgE-mediated activation of human eosinophils.

作者信息

Arock M, Le Goff L, Bécherel P A, Dugas B, Debré P, Mossalayi M D

机构信息

Groupe d'Immuno-Hématologie Moléculaire, CNRS URA625, CHU Pitié-Salpêtrière, Paris, France.

出版信息

Biochem Biophys Res Commun. 1994 Aug 30;203(1):265-71. doi: 10.1006/bbrc.1994.2177.

Abstract

Eosinophils display various receptors for immunoglobulin E (IgE) including the high affinity receptor for IgE (Fc epsilon RI), CD23 (Fc epsilon RII), and Mac-2/epsilon BP. We attempted here to clarify the role of these receptors in IgE-mediated activation of eosinophils from normal human bone marrow cultures. Pretreatment of eosinophils with IL-4 is required for IgE/anti-IgE-mediated stimulation of TNF-alpha and peroxydes production. TNF-alpha release from eosinophils was also induced following ligation of CD23 and to a lesser extent with anti-Mac-2, while Fc epsilon RI-ligation had no effect. IgE/anti-IgE effect dramatically decreased when eosinophils were pretreated with Fab fragments of CD23-mAb. In addition, this effect could also be reversed by inhibiting CD23-dependent nitric oxide pathway by NG-monomethyl-L-arginine. Nitric oxide chemical donor, SIN-1, induced TNF-alpha release from eosinophils. CD23 and nitric oxide pathway are thus involved in IgE-mediated stimulation of normodense human eosinophils.

摘要

嗜酸性粒细胞表达多种免疫球蛋白E(IgE)受体,包括IgE高亲和力受体(FcεRI)、CD23(FcεRII)和Mac-2/εBP。我们在此试图阐明这些受体在IgE介导的正常人骨髓培养嗜酸性粒细胞激活中的作用。IgE/抗IgE介导的肿瘤坏死因子-α(TNF-α)刺激和过氧化物产生需要用白细胞介素-4(IL-4)预处理嗜酸性粒细胞。CD23连接后也可诱导嗜酸性粒细胞释放TNF-α,抗Mac-2诱导的程度较小,而FcεRI连接则无作用。当用CD23单克隆抗体的Fab片段预处理嗜酸性粒细胞时,IgE/抗IgE效应显著降低。此外,通过用NG-单甲基-L-精氨酸抑制CD23依赖性一氧化氮途径,这种效应也可以逆转。一氧化氮化学供体SIN-1可诱导嗜酸性粒细胞释放TNF-α。因此,CD23和一氧化氮途径参与了IgE介导的正常密度人嗜酸性粒细胞刺激。

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