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Fcγ受体介导的对小鼠B细胞活化的抑制作用的亚类特异性

Subclass specificity of Fc gamma receptor-mediated inhibition of mouse B cell activation.

作者信息

Phillips N E, Parker D C

出版信息

J Immunol. 1985 May;134(5):2835-8.

PMID:3156919
Abstract

We have shown previously that cross-linking receptors for the Fc of IgG (Fc gamma R) to membrane Ig will inhibit membrane Ig-dependent mouse B cell activation. In this report we have determined which mouse IgG subclasses will mediate this inhibition by using monoclonal mouse anti-p-azophenylarsonate (anti-ars) antibodies to inhibit B cell activation by arsanilated rabbit Fab'2 anti-mouse IgM (arsFab'2 anti-mu). Cell recovery and Ig secretion after 4 days of culture with soluble helper factors and arsFab'2 anti-mu was inhibited by IgG1, IgG2b, and IgG2a anti-ars, but not IgM or Fab'2 anti-ars. In addition, we determined which of the inhibitory IgG subclasses are blocked by the monoclonal anti-mouse Fc gamma R antibody 2.4G2, which we have previously shown prevents inhibition by rabbit IgG anti-mu. These experiments demonstrated that 2.4G2 Fab could block inhibition mediated by IgG2a as well as that mediated by IgG1 and IgG2b. Because it has been reported that 2.4G2 does not bind the IgG2a receptor on macrophages, these data support our previous experiments, which indicated that this inhibition is not macrophage dependent.

摘要

我们之前已经表明,将IgG的Fc(FcγR)受体与膜Ig交联会抑制膜Ig依赖性小鼠B细胞的激活。在本报告中,我们通过使用单克隆小鼠抗对氨基苯砷酸盐(抗砷)抗体来抑制经砷酸处理的兔Fab'2抗小鼠IgM(砷酸Fab'2抗μ)激活B细胞,从而确定了哪些小鼠IgG亚类会介导这种抑制作用。用可溶性辅助因子和砷酸Fab'2抗μ培养4天后,细胞恢复和Ig分泌受到IgG1、IgG2b和IgG2a抗砷的抑制,但不受IgM或Fab'2抗砷的抑制。此外,我们确定了哪些抑制性IgG亚类会被单克隆抗小鼠FcγR抗体2.4G2阻断,我们之前已经表明该抗体可阻止兔IgG抗μ的抑制作用。这些实验表明,2.4G2 Fab可以阻断由IgG2a介导的抑制作用以及由IgG1和IgG2b介导的抑制作用。因为据报道2.4G2不与巨噬细胞上的IgG2a受体结合,所以这些数据支持了我们之前的实验,表明这种抑制作用不依赖于巨噬细胞。

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