| B cells limit repair after ischemic acute kidney injury. | |
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MedLine Citation:
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PMID: 20203156 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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Hye Ryoun Jang; Maria Teresa Gandolfo; Gang Jee Ko; Shailesh R Satpute; Lorraine Racusen; Hamid Rabb |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2010-03-04 |
Journal Detail:
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Title: Journal of the American Society of Nephrology : JASN Volume: 21 ISSN: 1533-3450 ISO Abbreviation: J. Am. Soc. Nephrol. Publication Date: 2010 Apr |
Date Detail:
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Created Date: 2010-04-01 Completed Date: 2010-04-22 Revised Date: 2011-07-27 |
Medline Journal Info:
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Nlm Unique ID: 9013836 Medline TA: J Am Soc Nephrol Country: United States |
Other Details:
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Languages: eng Pagination: 654-65 Citation Subset: IM |
Affiliation:
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Division of Nephrology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Acute Kidney Injury
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etiology*,
immunology Animals B-Lymphocytes / cytology, physiology* Cell Differentiation Cell Movement Interleukin-6 Receptor alpha Subunit / biosynthesis Mice Plasma Cells / cytology, immunology Reperfusion Injury / complications* |
| Grant Support | |
ID/Acronym/Agency:
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R01DK054770/DK/NIDDK NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Interleukin-6 Receptor alpha Subunit |
| Comments/Corrections | |
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