title: B cells limit repair after ischemic acute kidney injury.
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 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.
authors.affiliation: Division of Nephrology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
authors.forename: Hye Ryoun
authors.initials: HR
authors.lastname: Jang
authors.forename: Maria Teresa
authors.initials: MT
authors.lastname: Gandolfo
authors.forename: Gang Jee
authors.initials: GJ
authors.lastname: Ko
authors.forename: Shailesh R
authors.initials: SR
authors.lastname: Satpute
authors.forename: Lorraine
authors.initials: L
authors.lastname: Racusen
authors.forename: Hamid
authors.initials: H
authors.lastname: Rabb
mesh_terms: 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*
chemical_list: D053698:Interleukin-6 Receptor alpha Subunit