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DC Field | Value | Language |
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dc.contributor.author | Nozaki Y. | en |
dc.contributor.author | Richard Kitching A. | en |
dc.contributor.author | Akiba H. | en |
dc.contributor.author | Yagita H. | en |
dc.contributor.author | Kinoshita K. | en |
dc.contributor.author | Funauchi M. | en |
dc.contributor.author | Matsumura I. | en |
dc.date.accessioned | 2021-05-14T14:24:27Z | en |
dc.date.available | 2021-05-14T14:24:27Z | en |
dc.date.copyright | 2014 | en |
dc.date.created | 20140602 | en |
dc.date.issued | 2014-06-02 | en |
dc.identifier.citation | American Journal of Physiology - Renal Physiology. 306 (10) (pp F1210-F1221), 2014. Date of Publication: 2014. | en |
dc.identifier.issn | 0363-6127 | en |
dc.identifier.uri | https://repository.monashhealth.org/monashhealthjspui/handle/1/41997 | en |
dc.description.abstract | The T-cell immunoglobulin mucin 1, also known as kidney injury molecule-1, modulates CD4+ T-cell responses and is also expressed by damaged proximal tubules within the kidney. Both Th subset imbalance (Th1/Th2/Th17) and regulatory T-cell and B-cell alterations contribute to the pathogenesis of autoimmune disease. This study investigated the effects of an inhibitory anti-T-cell immunoglobulin mucin 1 antibody (RMT1-10) in lupus-prone MRL-Faslpr mice. MRL-Faslpr mice were treated with RMT1-10 or a control antibody intraperitoneally twice weekly from 3 mo of age for 16 wk. RMT1-10 treatment significantly improved survival, limited the development of lymphadenopathy and skin lesions, preserved renal function and decreased proteinuria, reduced serum anti-DNA antibody levels, and attenuated renal leukocyte accumulation. Th1 and Th17 cellular responses systemically and intrarenally were reduced, but regulatory T and B cells were increased. RMT1-10 treatment also reduced glomerular immunoglobulin and C3 deposition and suppressed cellular proliferation and apoptosis. Urinary excretion and renal expression of kidney injury molecule-1 was reduced, reflecting diminished interstitial injury. As RMT1-10 attenuated established lupus nephritis, manipulating immune system T-cell immunoglobulin mucin 1 may represent a therapeutic strategy in autoimmune diseases affecting the kidney. © 2014 the American Physiological Society. | en |
dc.language | en | en |
dc.language | English | en |
dc.publisher | American Physiological Society (E-mail: subscrip@the-aps.org) | en |
dc.relation.ispartof | American Journal of Physiology - Renal Physiology | en |
dc.title | Endogenous Tim-1 promotes severe systemic autoimmunity and renal disease MRL-Faslpr mice. | en |
dc.type | Article | en |
dc.identifier.doi | http://monash.idm.oclc.org/login?url=http://dx.doi.org/10.1152/ajprenal.00570.2013 | en |
dc.publisher.place | United States | en |
dc.identifier.pubmedid | 24623145 [http://www.ncbi.nlm.nih.gov/pubmed/?term=24623145] | en |
dc.identifier.source | 373104326 | en |
dc.identifier.institution | (Nozaki, Kinoshita, Funauchi, Matsumura) Department of Hematology and Rheumatology, Kinki University School of Medicine, Osaka, Japan (Richard Kitching) Centre for Inflammatory Diseases, Monash University Department of Medicine, Clayton, VIC, Australia (Richard Kitching) Departments of Nephrology and Pediatric Nephrology, Monash Medical Centre, Clayton, VIC, Australia (Akiba, Yagita) Department of Immunology, Juntendo University School of Medicine, Tokyo, Japan | en |
dc.description.address | Y. Nozaki, Dept. of Hematology and Rheumatology, Kinki Univ. School of Medicine, 377-2 Ohno-Higashi, Osaka-Sayama, Osaka 589-8511, Japan. E-mail: yuji0516@med.kindai.ac.jp | en |
dc.description.publicationstatus | Embase | en |
dc.rights.statement | Copyright 2014 Elsevier B.V., All rights reserved. | en |
dc.subect.keywords | Chemokine Cytokine Lupus nephritis Tim-1 | en |
dc.identifier.authoremail | Nozaki Y.; yuji0516@med.kindai.ac.jp | en |
item.openairecristype | http://purl.org/coar/resource_type/c_18cf | - |
item.cerifentitytype | Publications | - |
item.openairetype | Article | - |
item.grantfulltext | none | - |
item.fulltext | No Fulltext | - |
Appears in Collections: | Articles |
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