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dc.contributor.authorNagano, H
dc.contributor.authorMitchell, Richard Neal
dc.contributor.authorTaylor, M K
dc.contributor.authorHasegawa, S
dc.contributor.authorTilney, N L
dc.contributor.authorLibby, Peter
dc.date.accessioned2014-12-10T22:00:13Z
dc.date.issued1997
dc.identifier.citationNagano, H, R N Mitchell, M K Taylor, S Hasegawa, N L Tilney, and P Libby. 1997. “Interferon-Gamma Deficiency Prevents Coronary Arteriosclerosis but Not Myocardial Rejection in Transplanted Mouse Hearts.” J. Clin. Invest. 100 (3) (August 1): 550–557. doi:10.1172/jci119564.en_US
dc.identifier.issn0021-9738en_US
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:13497072
dc.description.abstractWe have hypothesized that T cell cytokines participate in the pathogenesis of graft arterial disease (GAD). This study tested the consequences of IFN-gamma deficiency on arterial and parenchymal pathology in murine cardiac allografts. Hearts from C-H-2(bm12)KhEg (bm12, H-2(bm12)) were transplanted into C57/B6 (B6, H-2(b)), wild-type, or B6 IFN-gamma-deficient (GKO) recipients after immunosuppression by treatment with anti-CD4 and anti-CD8 mAbs. In wild-type recipients, myocardial rejection peaked at 4 wk, (grade 2. 1+/-0.3 out of 4, mean+/-SEM, n = 9), and by 8-12 wk evolved coronary arteriopathy. At 12 wk, the GAD score was 1.4+/-0.3, and the parenchymal rejection grade was 1.2+/-0.3 (n = 8). In GKO recipients of bm12 allografts, myocardial rejection persisted at 12 wk (grade 2.5+/-0.3, n = 6), but no GAD developed (score: 0.0+/-0.0, n = 6, P < 0.01 vs. wild-type). Mice treated with anti-IFN-gamma mAbs showed similar results. Isografts generally showed no arterial changes. In wild-type recipients, arterial and parenchymal cells showed increased MHC class II molecules, intercellular adhesion molecule-1, and vascular cell adhesion molecule-1 compared to normal or isografted hearts. The allografts in GKO recipients showed attenuated expression of these molecules (n = 6). Thus, development of GAD, but not parenchymal rejection, requires IFN-gamma. Reduced expression of MHC antigens and leukocyte adhesion molecules may contribute to the lack of coronary arteriopathy in hearts allografted into GKO mice.en_US
dc.language.isoen_USen_US
dc.publisherAmerican Society for Clinical Investigationen_US
dc.relation.isversionofdoi:10.1172/JCI119564en_US
dc.relation.hasversionhttp://www.ncbi.nlm.nih.gov/pubmed/9239401en_US
dash.licenseLAA
dc.subjectarteriosclerosisen_US
dc.subjectcardiac transplantationen_US
dc.subjectIFN-g knockout mouseen_US
dc.titleInterferon-gamma deficiency prevents coronary arteriosclerosis but not myocardial rejection in transplanted mouse heartsen_US
dc.typeJournal Articleen_US
dc.description.versionVersion of Recorden_US
dc.relation.journalJournal of Clinical Investigationen_US
dash.depositing.authorLibby, Peter
dc.date.available2014-12-10T22:00:13Z
dc.identifier.doi10.1172/JCI119564*
dash.contributor.affiliatedMitchell, Richard
dash.contributor.affiliatedLibby, Peter
dc.identifier.orcid0000-0002-1502-502X


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