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Effects of Combined T‐ and B‐Cell Deficiency on Murine Ischemia Reperfusion Injury
Author(s) -
BurneTaney Melissa J.,
YokotaIkeda Naoko,
Rabb Hamid
Publication year - 2005
Publication title -
american journal of transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.89
H-Index - 188
eISSN - 1600-6143
pISSN - 1600-6135
DOI - 10.1111/j.1600-6143.2005.00815.x
Subject(s) - medicine , adoptive cell transfer , pathogenesis , kidney , immunology , t cell , reperfusion injury , b cell , acute kidney injury , ischemia , immune system , renal ischemia , antibody
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.

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