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The antiinflammatory activity of IgG: the intravenous IgG paradox Nimmerjahn F; Ravetch JVJ Exp Med 2007[Jan]; 204 (1): 11-5How 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.|Animals[MESH]|Anti-Inflammatory Agents/administration & dosage/chemistry/*pharmacology[MESH]|Autoimmune Diseases/immunology/therapy[MESH]|Humans[MESH]|Immunoglobulins, Intravenous/administration & dosage/chemistry/*pharmacology[MESH]|Macrophages/immunology[MESH]|Models, Immunological[MESH]|Receptors, IgG/metabolism[MESH]|Sialic Acids/chemistry[MESH] |
