Author:
Nimmerjahn Falk,Ravetch Jeffrey V.
Abstract
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 Fcγ receptor (FcγR), thereby protecting against autoantibody-mediated pathology.
Publisher
Rockefeller University Press
Subject
Immunology,Immunology and Allergy
Cited by
231 articles.
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