Naturally occurring autoantibodies mediate ischemia/reperfusion-induced tissue injury.
Ischemia and reperfusion events within the heart and brain and similar trauma-induced ischemia/reperfusion events lead to significant morbidity and mortality. In the past two decades, an excessive innate immune response has been identified as the mediator of reperfusion-induced tissue damage. Recent evidence indicates that naturally occurring autoantibody (NAb) activation of complement is a major mechanism of injury due to ischemia/reperfusion. This chapter focuses on the antigens exposed by ischemia and recognized by NAbs, the mechanism of complement activation by damaging NAbs and the protective role of IVIG in ischemia/reperfusion-induced pathology.
Division of Biology, Kansas State University, Manhattan, Kansas, USA. sdflemin@ksu.edu
Sherry D
SD
Fleming
D000818:Animals; D017152:Antibodies, Antiphospholipid / Q000276:immunology*; D001323:Autoantibodies / Q000276:immunology*; D001324:Autoantigens / Q000276:immunology; D003167:Complement Activation / Q000276:immunology; D003165:Complement System Proteins / Q000276:immunology; D006801:Humans; D007113:Immunity, Innate; D016756:Immunoglobulins, Intravenous / Q000276:immunology / Q000627:therapeutic use; D051379:Mice; D018345:Mice, Knockout; D015427:Reperfusion Injury / Q000276:immunology / Q000517:prevention & control*; D017412:Ribonucleoprotein, U1 Small Nuclear / Q000276:immunology; D053482:beta 2-Glycoprotein I / Q000276:immunology
D017152:Antibodies, Antiphospholipid; D001323:Autoantibodies; D001324:Autoantigens; D016756:Immunoglobulins, Intravenous; D017412:Ribonucleoprotein, U1 Small Nuclear; D053482:beta 2-Glycoprotein I; D003165:Complement System Proteins