The antiinflammatory activity of IgG: the intravenous IgG paradox.
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.
Nimmerjahn
Falk
F
Laboratory of Molecular Genetics and Immunology, The Rockefeller University, New York, NY 10021, USA.
Ravetch
Jeffrey V
JV
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000008:administration & dosage / Q000737:chemistry / Q000494:pharmacology*; D001327:Autoimmune Diseases / Q000276:immunology / Q000628:therapy; D006801:Humans; D016756:Immunoglobulins, Intravenous / Q000008:administration & dosage / Q000737:chemistry / Q000494:pharmacology*; D008264:Macrophages / Q000276:immunology; D018448:Models, Immunological; D017452:Receptors, IgG / Q000378:metabolism; D012794:Sialic Acids / Q000737:chemistry
D000893:Anti-Inflammatory Agents; D016756:Immunoglobulins, Intravenous; D017452:Receptors, IgG; D012794:Sialic Acids