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The antiinflammatory activity of IgG: the intravenous IgG paradox

Falk Nimmerjahn1, Jeffrey V Ravetch

  • 1Laboratory of Molecular Genetics and Immunology, The Rockefeller University, New York, NY 10021, USA.

The Journal of Experimental Medicine
|January 18, 2007
PubMed

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 Fcgamma receptor (FcgammaR), thereby protecting against autoantibody-mediated pathology.

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