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 Fcgamma receptor (FcgammaR), thereby protecting against autoantibody-mediated pathology.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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Anti-Inflammatory Agents / administration & dosage
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Anti-Inflammatory Agents / chemistry
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Anti-Inflammatory Agents / pharmacology*
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Autoimmune Diseases / immunology
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Autoimmune Diseases / therapy
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Humans
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Immunoglobulins, Intravenous / administration & dosage
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Immunoglobulins, Intravenous / chemistry
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Immunoglobulins, Intravenous / pharmacology*
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Macrophages / immunology
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Models, Immunological
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Receptors, IgG / metabolism
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Sialic Acids / chemistry
Substances
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Anti-Inflammatory Agents
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Immunoglobulins, Intravenous
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Receptors, IgG
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Sialic Acids