The antiinflammatory activity of IgG: the intravenous IgG paradox

被引：217

作者：

Nimmerjahn, Falk ^{[1
]}

Ravetch, Jeffrey V. ^{[1
]}

机构：

[1] Rockefeller Univ, Lab Mol Genet & Immunol, New York, NY 10021 USA

来源：

JOURNAL OF EXPERIMENTAL MEDICINE | 2007年 / 204卷 / 01期

关键词：

D O I：

10.1084/jem.20061788

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

How high doses of intravenous IgG (IVIG) suppress autoimmune diseases remains unresolved. We have recently shown that the antiinflammatory activity of IVIG can be attributed to a minor species of IgGs that is modified with terminal sialic acids on their Fc-linked glycans. Here we propose that these Fc-sialylated IgGs engage a unique receptor on macrophages that, in turn, leads to the upregulation of an inhibitory Fc gamma receptor (Fc gamma R), thereby protecting against autoantibody-mediated pathology.

引用

页码：11 / 15

页数：5

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