What is the physiology of intravenous immunoglobulin (IVIG) activation?

Updated: Jul 05, 2018
  • Author: Jessica Katz, MD, PhD, FACP; Chief Editor: Emmanuel C Besa, MD  more...
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Answer

Answer

IVIG is an immunomodulating agent that has multiple activities. These include modulation of complement activation; suppression of idiotypic antibodies; saturation of Fc receptors on macrophages; and suppression of various inflammatory mediators, including cytokines, chemokines, and metalloproteinases. [5] Fc receptors are a class of receptors on immune cells that bind to the Fc (constant region) portion of an antibody. The Fc region of IgG facilitates interaction with and signaling through Fc receptors on antigen presenting cells such as phagocytes, B cells, and other cells and with Fc-binding plasma proteins (eg, components of the complement system). [6]

Blockade of macrophage Fc receptors is considered the primary mechanism of action of immune globulin in persons with ITP and other autoantibody-mediated cytopenias. In persons with Kawasaki disease and dermatomyositis, IVIG is thought to inhibit the generation of membrane attack complexes (C5b-C9) and subsequent complement-mediated tissue damage by binding the activated components C3b and C4b, thus preventing their deposition on target surfaces. In persons with dermatomyositis, IVIG induces a decrease in the plasma levels of membrane attack complex and a substantial decrease in the amounts of C3b and membrane attack complex deposited in endomysial capillaries. The high content of anti-idiotypes against autoantibodies in IVIG facilitates its ability to neutralize autoantibodies, as is shown in patients with acquired hemophilia due to autoantibodies against factor VIII. [6]


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