Author(s): Ballow M
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Abstract Intravenous immune globulin (IVIG) is an important treatment modality in patients with humoral or B-cell immune deficiency as replacement therapy. Soon after its introduction in the early 1980s for the treatment of patients with immune deficiency, IVIG was used in the treatment of children with idiopathic thrombocytopenia purpura. Presently, more commercial IVIG is used for the treatment of autoimmune and inflammatory disorders than as replacement therapy in patients with immune deficiency. Understanding the mechanisms of action of IVIG in these autoimmune and inflammatory disorders has occupied investigators over the past 3 decades. A number of mechanisms for the immune modulation and anti-inflammatory actions of IVIG have been described, including Fc receptor blockade, inhibition of complement deposition, enhancement of regulatory T cells, inhibition or neutralization of cytokines and growth factors, accelerated clearance of autoantibodies, modulation of adhesion molecules and cell receptors, and activation of regulatory macrophages through the FcγRIIb receptor. It can now be appreciated that IVIG affects many different pathways to modulate the immune and inflammatory response. Further delineation of these pathways might lead to new treatment strategies. Copyright © 2010 American Academy of Allergy, Asthma & Immunology. Published by Mosby, Inc. All rights reserved.
This article was published in J Allergy Clin Immunol
and referenced in Biochemistry & Analytical Biochemistry