Autoimmune diseases are characterized by the production of autoantibodies specific for self-antigens by activated B cells. However, the precise mechanism for the pathogenesis of autoimmunity remains unknown. Intravenous immunoglobulin (IVIg), which is manufactured from the pooled plasma of more than tens of thousands of healthy volunteers, is used successfully for the treatment of inflammatory and autoimmune disease, especially in case of resistance to conventional therapy such as steroid pulse therapy. Although the precise mechanisms by which IVIg acts in the treatment of autoimmune disease remain unclear, several groups have proposed various mechanisms that could play a role in modulating undesirable autoimmune responses. The IgG molecules in IVIg have various immunosuppressive effects, which are attributed to the Fc portion or antigen recognition region. Herein, I focus on the immunosuppressive effects of IVIg on activated B cells, mediated by the antigen recognition region.