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DC Field | Value | Language |
---|---|---|
dc.contributor.author | Li S. | en |
dc.contributor.author | Holdsworth S.R. | en |
dc.contributor.author | Tipping P.G. | en |
dc.date.accessioned | 2021-05-14T11:18:48Z | en |
dc.date.available | 2021-05-14T11:18:48Z | en |
dc.date.copyright | 2000 | en |
dc.date.created | 20010103 | en |
dc.date.issued | 2012-10-22 | en |
dc.identifier.citation | Clinical and Experimental Immunology. 122 (3) (pp 453-458), 2000. Date of Publication: 2000. | en |
dc.identifier.issn | 0009-9104 | en |
dc.identifier.uri | https://repository.monashhealth.org/monashhealthjspui/handle/1/33365 | en |
dc.description.abstract | MHC II and CD4+ T cells are required for anti-glomerular basement membrane (GBM) globulininitiated crescentic glomerulonephritis (GN) in mice, but the role of MHC I and CD8+ T cells is unclear. The cytolytic function of CD8+ T cells requires recognition of peptide antigens presented on MHC I. CD8+ T cells can also perform helper functions via cytokine production. The contribution of MHC I to crescentic GN was investigated using TAP-1 gene knock out (TAP-1-/-) mice, which have deficient MHC I antigen presentation. Heterozygous TAP-1 mice have normal MHC I expression and developed GN with crescents in 42 +/- 4% of glomeruli (normal 0%), proteinuria (9.1 +/- 1.6 mg/20 h, normal 1.5 +/- 0.3 mg/20 h) and impaired renal function (creatinine clearance 110 +/- 8 mul/min, normal 193 +/- 10 mul/min) following administration of sheep anti-mouse GBM globulin. TAP-1-/- mice, which have extremely low MHC I expression and reduced CD8+ T cells, developed similar GN with 39 +/- 3% crescents, proteinuria (12.7 +/- 4.3 mg/20 h) and impaired renal function (creatinine clearance 123 +/- 20 mul/min). In vivo antibody-induced CD8 depletion did not attenuate crescent formation or protect renal function in C57B1/6 mice developing GN, although significant reduction in proteinuria (5.3 +/- 1.2 mg/20 h, P = 0.012) and glomerular recruitment of CD4+ T cells and macrophages were observed compared with control treated mice with GN. These data demonstrate that MHC I is not required for development of crescentic GN in mice. The MHC I-independent contribution of CD8+ T cells to proteinuria and inflammatory cell recruitment suggests that they may serve a 'helper' rather than cytolytic role in this disease. | en |
dc.language | en | en |
dc.language | English | en |
dc.publisher | Blackwell Publishing Ltd (9600 Garsington Road, Oxford OX4 2XG, United Kingdom) | en |
dc.title | MHC class I pathway is not required for the development of crescentic glomerulonephritis in mice. | en |
dc.type | Article | en |
dc.identifier.doi | http://monash.idm.oclc.org/login?url=http://dx.doi.org/10.1046/j.1365-2249.2000.01387.x | en |
dc.publisher.place | United Kingdom | en |
dc.identifier.pubmedid | 11122254 [http://www.ncbi.nlm.nih.gov/pubmed/?term=11122254] | en |
dc.identifier.source | 32002206 | en |
dc.identifier.institution | (Li, Holdsworth, Tipping) Centre for Inflammatory Diseases, Monash University, Department of Medicine, Clayton, Vic., Australia (Tipping) Department of Medicine, Monash Medical Centre, 246 Clayton Road, Clayton, Vic. 3168, Australia | en |
dc.description.address | P.G. Tipping, Department of Medicine, Monash Medical Centre, 246 Clayton Road, Clayton, Vic. 3168, Australia. E-mail: peter.tipping@med.monash.edu.au | en |
dc.description.publicationstatus | Embase | en |
dc.rights.statement | Copyright 2012 Elsevier B.V., All rights reserved. | en |
dc.subect.keywords | CD8 Macrophage T cell TAP-1 | en |
dc.identifier.authoremail | Tipping P.G.; peter.tipping@med.monash.edu.au | en |
item.fulltext | No Fulltext | - |
item.grantfulltext | none | - |
item.cerifentitytype | Publications | - |
item.openairetype | Article | - |
item.openairecristype | http://purl.org/coar/resource_type/c_18cf | - |
crisitem.author.dept | Immunology and Allergy | - |
Appears in Collections: | Articles |
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