The complement system, consisting of soluble and cell membrane–bound components of
the innate immune system, has defined roles in the pathophysiology of renal allograft
rejection. Notably, the unavoidable ischemia-reperfusion injury inherent to transplantation is
mediated through the terminal complement activation products C5a and C5b-9.
Furthermore, biologically active fragments C3a and C5a, produced during complement
activation, can modulate both antigen presentation and T cell priming, ultimately leading to …