Abstract

Antibodies are well known for their role in humoral immunity, and their prominent involvement in the protection afforded by successful vaccines against infections. A less appreciated function of antibodies is their capacity to dampen the autoimmune responses associated with some inflammatory diseases. Nevertheless, this paradoxical activity of antibodies is used to treat patients with autoimmune disease. Preparations of polyclonal serum IgG, which are obtained from pools of thousands of human blood donors and are called intravenous immunoglobulin (IVIg), are commonly used to treat patients suffering from immunothrombocytopenia. Although of important clinical significance the anti-inflammatory function of polyclonal IgG remains poorly understood. Previous studies have primarily addressed its mode of action in a prophylactic setting. However, IVIg is usually applied therapeutically in the clinic. In a study published in this issue of the European Journal of Immunology, Schwab et al. [Eur. J. Immunol. 2014. 44: 1444-1453] focus specifically on the protective effect of IVIg in a therapeutic setting, in four different mouse models of autoantibody-mediated pathology, in order to better approach the condition in human disease and therapy. This Commentary discusses how their findings have key implications for our understanding, and further deciphering, of the mode of action of this therapy.

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