The pathogenesis of ischemia–reperfusion injury (IRI) is complex and not well understood.
Inflammation plays an important role in IRI, with involvement of leukocytes, adhesion
molecules, chemokines and cytokines. Emerging data suggest a role of T cells as mediators
of IRI both in renal and extra-renal organs. Divergent roles of T cell subsets have also been
elucidated, suggesting a more complicated role of T cells in the different phases of IRI. This
review presents recent evidence from various animal models that advances our …