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DC Field | Value | Language |
---|---|---|
dc.contributor.author | Dewage L. | en |
dc.contributor.author | Kitching A.R. | en |
dc.contributor.author | Holdsworth S.R. | en |
dc.contributor.author | Summers S.A. | en |
dc.contributor.author | Phoon R.K.S. | en |
dc.contributor.author | Odobasic D. | en |
dc.date.accessioned | 2021-05-14T10:15:21Z | en |
dc.date.available | 2021-05-14T10:15:21Z | en |
dc.date.copyright | 2011 | en |
dc.date.created | 20111019 | en |
dc.date.issued | 2012-10-08 | en |
dc.identifier.citation | Clinical and Experimental Immunology. 166 (2) (pp 227-234), 2011. Date of Publication: November 2011. | en |
dc.identifier.issn | 0009-9104 | en |
dc.identifier.uri | https://repository.monashhealth.org/monashhealthjspui/handle/1/30340 | en |
dc.description.abstract | Experimental crescentic glomerulonephritis is driven by systemic cellular immune responses. A pathogenic role for T helper type 1 (Th1) and Th17 cells is well established. T-bet, a key transcription factor required for Th1 lineage commitment, and retinoic acid-related orphan receptor-gammat (Rorgammat), a key Th17 transcription factor, are required for full expression of disease. Similarly, several Th1- and Th17-associated cytokines have been implicated in disease augmentation. The role of Th2 cells in the disease is less clear, although Th2-associated cytokines, interleukin (IL)-4 and IL-10, are protective. We sought to determine the role of signal transducer and activation of transcription 6 (STAT6), a key regulator of Th2 responses, in experimental crescentic glomerulonephritis. Compared to wild-type mice, histological and functional renal injury was enhanced significantly in STAT6-/- mice 21 days after administration of sheep anti-mouse glomerular basement membrane globulin. Consistent with the enhanced renal injury, both Th1 and Th17 nephritogenic immune responses were increased in STAT6-/- mice. Conversely, production of IL-5, a key Th2-associated cytokine, was decreased significantly in STAT6-/- mice. Early in the disease process systemic mRNA expression of T-bet and Rorgamma was increased in STAT6-/- mice. We conclude that STAT6 is required for attenuation of Th1 and Th17 nephritogenic immune responses and protection from crescentic glomerulonephritis. © 2011 The Authors. Clinical and Experimental Immunology © 2011 British Society for Immunology. | en |
dc.language | English | en |
dc.language | en | en |
dc.publisher | Blackwell Publishing Ltd (9600 Garsington Road, Oxford OX4 2XG, United Kingdom) | en |
dc.title | Signal transducer and activation of transcription 6 (STAT6) regulates T helper type 1 (Th1) and Th17 nephritogenic immunity in experimental crescentic glomerulonephritis. | en |
dc.type | Article | en |
dc.identifier.doi | http://monash.idm.oclc.org/login?url=http://dx.doi.org/10.1111/j.1365-2249.2011.04437.x | en |
dc.publisher.place | United Kingdom | en |
dc.identifier.pubmedid | 21985369 [http://www.ncbi.nlm.nih.gov/pubmed/?term=21985369] | en |
dc.identifier.source | 362714166 | en |
dc.identifier.institution | (Summers, Phoon, Odobasic, Dewage, Kitching, Holdsworth) Centre for Inflammatory Diseases, Monash University, Department of Medicine, Australia (Summers, Kitching, Holdsworth) Department of Nephrology, Monash Medical Centre, Clayton, VIC, Australia | en |
dc.description.address | S.R. Holdsworth, Centre for Inflammatory Diseases, Monash University Department of Medicine, Monash Medical Centre, 246 Clayton Road, Clayton, VIC 3168, Australia. E-mail: stephen.holdsworth@monash.edu | en |
dc.description.publicationstatus | Embase | en |
dc.rights.statement | Copyright 2012 Elsevier B.V., All rights reserved. | en |
dc.subect.keywords | Glomerulonephritis Renal immunology/disease T cells | en |
dc.identifier.authoremail | Holdsworth S.R.; stephen.holdsworth@monash.edu | en |
item.openairecristype | http://purl.org/coar/resource_type/c_18cf | - |
item.cerifentitytype | Publications | - |
item.openairetype | Article | - |
item.grantfulltext | none | - |
item.fulltext | No Fulltext | - |
crisitem.author.dept | Nephrology | - |
crisitem.author.dept | Immunology and Allergy | - |
Appears in Collections: | Articles |
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