B cells limit repair after ischemic acute kidney injury.
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 muMT (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 muMT 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 muMT 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.
Jang
Hye Ryoun
HR
Division of Nephrology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Gandolfo
Maria Teresa
MT
Ko
Gang Jee
GJ
Satpute
Shailesh R
SR
Racusen
Lorraine
L
Rabb
Hamid
H
D058186:Acute Kidney Injury / Q000209:etiology* / Q000276:immunology; D000818:Animals; D001402:B-Lymphocytes / Q000166:cytology / Q000502:physiology*; D002454:Cell Differentiation; D002465:Cell Movement; D053698:Interleukin-6 Receptor alpha Subunit / Q000096:biosynthesis; D051379:Mice; D010950:Plasma Cells / Q000166:cytology / Q000276:immunology; D015427:Reperfusion Injury / Q000150:complications*
D053698:Interleukin-6 Receptor alpha Subunit