Journal
JOURNAL OF EXPERIMENTAL MEDICINE
Volume 204, Issue 1, Pages 11-15Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20061788
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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.
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