Related Experiment Video
Updated: Aug 18, 2026

A Murine Model of Myocardial Ischemia-reperfusion Injury through Ligation of the Left Anterior Descending Artery
Published on: April 10, 2014
Effects of combined T- and B-cell deficiency on murine ischemia reperfusion injury
Melissa J Burne-Taney1, Naoko Yokota-Ikeda, Hamid Rabb
1Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
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.
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.

