B cells limit repair after ischemic acute kidney injuryopen access
- Authors
- Jang H.R.; Gandolfo M.T.; Ko G.J.; Satpute S.R.; Racusen L.; Rabb H.
- Issue Date
- 2010
- Citation
- Journal of the American Society of Nephrology, v.21, no.4, pp 654 - 665
- Pages
- 12
- Indexed
- SCI
SCIE
SCOPUS
- Journal Title
- Journal of the American Society of Nephrology
- Volume
- 21
- Number
- 4
- Start Page
- 654
- End Page
- 665
- URI
- https://scholarworks.korea.ac.kr/kumedicine/handle/2020.sw.kumedicine/15507
- DOI
- 10.1681/ASN.2009020182
- ISSN
- 1046-6673
1533-3450
- 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. Copyright © 2010 by the American Society of Nephrology.
- Files in This Item
- There are no files associated with this item.
- Appears in
Collections - 2. Clinical Science > Department of Nephrology and Hypertension > 1. Journal Articles
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.