Intravenous immunoglobulins (IVIg) have been used as a substitutive treatment for primary and secondary humoral immune deficiencies for several decades. In the meantime, increased experience has been acquired with IVIg in the management of other inflammatory and autoimmune disorders, such as Kawasakis disease, idiopathic thrombocytopenic purpura, dermatomyositis or Guillain-Barre syndrome, in which several clinical trials have demonstrated its efficacy. In other pathologies, IVIg seem to be effective, although further studies are required. Nevertheless, the exact mechanism by which IVIg exert their beneficial actions is not completely understood. According to in vitro as well as in vivo data, several mechanisms of action have been proposed: Fc receptor blockade, idiotype-antiidiotype interactions, neutralisation of bacterial toxins and superantigens, competitive inhibition of complement activation, down-regulation of B- and T-cell function, enhancement of pathogenic autoantibodies clearance, modulation of soluble products, apoptosis blockade via Fas receptor and administration of soluble products which could interfere with the immune response. Both IVIg structure, as well as its obtention from pooled human plasma donors, seem to play an important role in IVIg immunomodulatory properties. Thus, the objective of the present article is to review the current evidence upon the mechanisms of action of IVIg.