Immunopathogenesis of ischemia/reperfusion-associated tissue damage

Abstract

Ischemia/reperfusion (IR) instigates a complex array of inflammatory events which result in damage to the local tissue. IR-related organ damage occurs invariably in several clinical conditions including trauma, organ transplantation, autoimmune diseases and revascularization procedures. We critically review available pre-clinical experimental information on the role of immune response in the expression of tissue damage following IR. Distinct elements of the innate and adaptive immune response are involved in the expression of tissue injury. Interventions such as prevention of binding of natural antibody to antigen expressed on the surface of ischemia-conditioned cells, inhibition of the ensuing complement activation, modulation of Toll-like receptors, B or T cell depletion and blockade of inflammatory cytokines and chemokines limit IR injury in preclinical studies. Clinical trials that will determine the therapeutic value of each approach is needed.