Institute of Genetics, Department of Biology, University of Erlangen-Nuremberg, Erlangen, Germany.
Eur J Immunol. 2012 Dec;42(12):3302-9. doi: 10.1002/eji.201242710. Epub 2012 Oct 16.
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.
静脉注射免疫球蛋白（IVIg）能够有效地抑制多种自身免疫性疾病。在过去的几年中，这种抗炎活性的潜在机制已经逐渐明朗。其中，免疫球蛋白 G 恒定片段糖部分的末端唾液酸残基被证明对于类风湿关节炎和免疫性血小板减少症（ITP）模型中的 IVIg 抗炎活性至关重要。最近，B 细胞和唾液酸结合蛋白 CD22 被认为参与了这种 IVIg 依赖性免疫调节途径。为了研究 B 细胞是否直接参与 IVIg 介导的急性自身免疫性疾病的抑制，我们在 B 细胞或 CD22 缺失的小鼠中测试了 IVIg 的活性。我们发现，无论是 B 细胞还是 CD22 对于 IVIg 在类风湿关节炎和 ITP 小鼠模型中的即时抗炎活性都不是必需的。
