The complement system, traditionally considered a component of innate immunity, is now recognized as a crucial mediator of the adaptive immune response in solid organ transplantation. Preclinical and early human trials have demonstrated the importance of complement effector mechanisms in driving allograft injury during specific antigraft immune responses, including ischemia-reperfusion injury, T-cell-mediated rejection, and antibody-mediated rejection, as well as a potential role for complement-derived risk stratification biomarkers. These data support the need for further testing of complement inhibitors in solid organ transplant recipients.
Keywords: Antibody-mediated rejection; Complement; Ischemia-reperfusion injury; T cells.
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