Immunomodulatory effect of immunoglobulins.
IVIG is clearly indicated as the treatment of choice on the basis of large clinical trials in a number of inflammatory and autoimmune diseases, e.g. Kawasaki disease, ITP, Guillain-Barré syndrome, etc. According to in vitro studies various mechanisms have been identified whereby IgG could modify immunologically mediated and inflammatory diseases. Fc-receptor blockade as well as true down-modulation of Fc-receptors, acting as a sump for activated complement components, have been demonstrated at the cellular level and in experimental animals. The possibility of interfering with the idiotype network has been discussed in connection with autoimmune diseases. Down-regulation of inflammatory cytokines as well as an increase in the production and release of IL-1 receptor antagonist appears to be of importance in inflammatory processes. Clinical studies have proven the efficacy of IVIG. Basic research has demonstrated its possible mechanisms of action; however, the question of exactly which mechanisms are responsible for the clinical efficacy in certain diseases still awaits clarification.
Wolf
H M
HM
Institute of Immunology, University of Vienna, Austria.
Eibl
M M
MM
D000818:Animals; D016207:Cytokines / Q000187:drug effects / Q000378:metabolism; D006801:Humans; D007154:Immune System Diseases / Q000188:drug therapy; D007109:Immunity / Q000502:physiology*; D007074:Immunoglobulin G / Q000494:pharmacology; D016756:Immunoglobulins, Intravenous / Q000276:immunology* / Q000627:therapeutic use*; D007249:Inflammation / Q000188:drug therapy; D053590:Interleukin 1 Receptor Antagonist Protein; D011961:Receptors, Fc / Q000502:physiology*; D012795:Sialoglycoproteins / Q000096:biosynthesis / Q000187:drug effects
D016207:Cytokines; C507763:IL1RN protein, human; D007074:Immunoglobulin G; D016756:Immunoglobulins, Intravenous; D053590:Interleukin 1 Receptor Antagonist Protein; D011961:Receptors, Fc; D012795:Sialoglycoproteins