Journal
EUROPEAN JOURNAL OF IMMUNOLOGY
Volume 42, Issue 12, Pages 3302-3309Publisher
WILEY
DOI: 10.1002/eji.201242710
Keywords
Autoimmune disease; B cells; CD22; Inflammation; IVIg
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Funding
- Bavarian Genome Research network (BayGene)
- Bill and Melinda Gates foundation [OPP1032817]
- Bill and Melinda Gates Foundation [OPP1032817] Funding Source: Bill and Melinda Gates Foundation
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Intravenous immunoglobulins (IVIgs) efficiently suppress a variety of autoimmune diseases. Over the past few years several potential mechanisms underlying this antiinflammatory activity have become apparent. Among these, terminal sialic acid residues in the sugar moiety of the immunoglobulin G constant fragment have been shown to be critical for the antiinflammatory activity of IVIgs in models of rheumatoid arthritis and immunothrombocytopenia (ITP). More recently, B cells and the sialic acid-binding protein CD22 were suggested to be involved in this IVIg-dependent immunomodulatory pathway. To study whether B cells are directly involved in IVIg-mediated suppression of acute autoimmune diseases, we tested the activity of IVIgs in mice deficient in B cells or CD22. We show that neither B cells nor CD22 are critical for the immediate antiinflammatory activity of IVIgs in mouse models of rheumatoid arthritis and ITP.
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