B cells limit repair after ischemic acute kidney injury

Hye Ryoun Jang, Maria Teresa Gandolfo, Gang Jee Ko, Shailesh R. Satpute, Lorraine Racusen, Hamid Rabb

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89 Citations (Scopus)


There is no established modality to repair kidney damage resulting from ischemia-reperfusion injury (IRI). Early responses to IRI involve lymphocytes, but the role of B cells in tissue repair after IRI is unknown. Here, we examined B cell trafficking into postischemic mouse kidneys and compared the repair response between control (wild-type) and μMT (B cell-deficient) mice with and without adoptive transfer of B cells. B cells infiltrated postischemic kidneys and subsequently activated and differentiated to plasma cells during the repair phase. Plasma cells expressing CD126 increased and B-1 B cells trafficked into postischemic kidneys with distinct kinetics. An increase in B lymphocyte chemoattractant in the kidney preceded B cell trafficking. Postischemic kidneys of μMT mice expressed higher IL-10 and vascular endothelial growth factor and exhibited more tubular proliferation and less tubular atrophy. Adoptive transfer of B cells into μMT mice reduced tubular proliferation and increased tubular atrophy. Treatment with anti-CD126 antibody increased tubular proliferation and reduced tubular atrophy in the late repair phase. These results demonstrate that B cells may limit the repair process after kidney IRI. Targeting B cells could have therapeutic potential to improve repair after IRI.

Original languageEnglish
Pages (from-to)654-665
Number of pages12
JournalJournal of the American Society of Nephrology
Issue number4
Publication statusPublished - 2010 Apr
Externally publishedYes

ASJC Scopus subject areas

  • General Medicine


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