B Cells Limit Repair after Ischemic Acute Kidney Injury : Journal of the American Society of Nephrology (original) (raw)

BASIC RESEARCH

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

*Nephrology Division, Department of Medicine, and

‡Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland; and

†Nephrology Division, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea

Correspondence: Dr. Hamid Rabb, Division of Nephrology, Johns Hopkins University School of Medicine, Ross Building, Room 965, 720 Rutland Avenue, Baltimore, MD 21205. Phone: 410-502-1555; Fax: 410-614-5129; E-mail: [email protected]

Received February 14, 2009

Accepted November 25, 2009

Abstract

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.