Abstract:
: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.
journal_name
Eur J Immunoljournal_title
European journal of immunologyauthors
Schwab I,Seeling M,Biburger M,Aschermann S,Nitschke L,Nimmerjahn Fdoi
10.1002/eji.201242710subject
Has Abstractpub_date
2012-12-01 00:00:00pages
3302-9issue
12eissn
0014-2980issn
1521-4141journal_volume
42pub_type
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