Intravenous immunoglobulin (IVIg) has been used for nearly three decades as an efficient anti-inflammatory therapeutic regimen in a growing number of autoimmune diseases. Despite this their success in clinical application, the mechanism of action of IVIg therapy remains elusive. During the last few years, several mechanisms dependent on either the IgG variable or constant fragment have been proposed to explain the potent immunomodulatory activity of IVIg. This review will discuss which molecular and cellular pathways might be involved in the anti-inflammatory activity of IVIg and for which types of autoimmune diseases they might be relevant.
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