B and T cells have been implicated in the pathogenesis of renal ischemia reperfusion injury (IRI); however, it is unknown if B and T cells interact in early injury responses, as seen in adaptive immune responses. Recent evidence has shown that B-cell deficient and T-cell deficient mice are partially protected from renal IRI. Renal IRI was induced in recombinase activating gene (RAG)-1 deficient mice, which lack both B and T cells. RAG-1 deficient mice from two different background strains were not protected from renal IRI. Adoptive transfer of either B or T cells into RAG-1 deficient mice led to a significant protection of renal injury, which was independent of effects on neutrophil trafficking. Neutrophil depletion in RAG-1 deficient mice did not protect from IRI. While deficiency of either B or T cells reduced IRI, combined lack of both is not protective. These results demonstrate that complex interactions between B and T cells are likely occurring in kidney IRI.