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- Publisher Website: 10.1161/01.RES.85.6.551
- Scopus: eid_2-s2.0-0033578663
- PMID: 10488058
- WOS: WOS:000082798600009
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Article: Susceptibility to myocarditis is dependent on the response of αβ T lymphocytes to coxsackieviral infection
Title | Susceptibility to myocarditis is dependent on the response of αβ T lymphocytes to coxsackieviral infection |
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Authors | |
Keywords | Cytokine Transgenic mice T lymphocyte Coxsackievirus Myocarditis |
Issue Date | 1999 |
Citation | Circulation Research, 1999, v. 85, n. 6, p. 551-558 How to Cite? |
Abstract | Viral myocarditis is an important cause of heart failure and dilated cardiomyopathy. T lymphocytes are implicated in myocardial damage in murine models of coxsackievirus B3 (CVB3) myocarditis. We used knockout mice lacking CD4 (CD4(-/-)), CD8 (CD8(-/-)), both coreceptors (CD4(-/-)CD8(-/-)), or the T-cell receptor β chain (TCRβ(-/-)) to address the contribution of T-cell subpopulations to host susceptibility to CVB3 myocarditis. Severity of disease was magnified in CD8(-/-) mice but attenuated in CD4(-/-) mice, consistent with a pathogenic role for CD4+ lymphocytes. Elimination of both CD4 and CD8 molecules from T lymphocytes by genetic knockout better protected mice from myocarditis, demonstrating that both CD4+ and CD8+ T cells contribute to host susceptibility. The same benefit occurred in TCRβ(-/-) mice, with prolonged survival and minimal myocardial disease observed after CVB3 infection. Elevated interferon-γ and decreased tumor necrosis factor-α expression are associated with attenuated myocardial damage in CD4(-/-)CD8(- /-) mice. These results show that the presence of TCRαβ+ T cells enhances host susceptibility to myocarditis. The severity of myocardial damage and associated mortality are dependent on the predominant T-cell type available to respond to CVB3 infection. One mechanism by which CD4+ and CD8+ T-cell subsets influence the pathogenesis of myocarditis may involve specific cytokine expression patterns. |
Persistent Identifier | http://hdl.handle.net/10722/291505 |
ISSN | 2023 Impact Factor: 16.5 2023 SCImago Journal Rankings: 4.903 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Opavsky, Mary Anne | - |
dc.contributor.author | Penninger, Josef | - |
dc.contributor.author | Aitken, Karen | - |
dc.contributor.author | Wen, Wen Hu | - |
dc.contributor.author | Dawood, Fayez | - |
dc.contributor.author | Mak, Tak | - |
dc.contributor.author | Liu, Peter | - |
dc.date.accessioned | 2020-11-17T14:54:31Z | - |
dc.date.available | 2020-11-17T14:54:31Z | - |
dc.date.issued | 1999 | - |
dc.identifier.citation | Circulation Research, 1999, v. 85, n. 6, p. 551-558 | - |
dc.identifier.issn | 0009-7330 | - |
dc.identifier.uri | http://hdl.handle.net/10722/291505 | - |
dc.description.abstract | Viral myocarditis is an important cause of heart failure and dilated cardiomyopathy. T lymphocytes are implicated in myocardial damage in murine models of coxsackievirus B3 (CVB3) myocarditis. We used knockout mice lacking CD4 (CD4(-/-)), CD8 (CD8(-/-)), both coreceptors (CD4(-/-)CD8(-/-)), or the T-cell receptor β chain (TCRβ(-/-)) to address the contribution of T-cell subpopulations to host susceptibility to CVB3 myocarditis. Severity of disease was magnified in CD8(-/-) mice but attenuated in CD4(-/-) mice, consistent with a pathogenic role for CD4+ lymphocytes. Elimination of both CD4 and CD8 molecules from T lymphocytes by genetic knockout better protected mice from myocarditis, demonstrating that both CD4+ and CD8+ T cells contribute to host susceptibility. The same benefit occurred in TCRβ(-/-) mice, with prolonged survival and minimal myocardial disease observed after CVB3 infection. Elevated interferon-γ and decreased tumor necrosis factor-α expression are associated with attenuated myocardial damage in CD4(-/-)CD8(- /-) mice. These results show that the presence of TCRαβ+ T cells enhances host susceptibility to myocarditis. The severity of myocardial damage and associated mortality are dependent on the predominant T-cell type available to respond to CVB3 infection. One mechanism by which CD4+ and CD8+ T-cell subsets influence the pathogenesis of myocarditis may involve specific cytokine expression patterns. | - |
dc.language | eng | - |
dc.relation.ispartof | Circulation Research | - |
dc.subject | Cytokine | - |
dc.subject | Transgenic mice | - |
dc.subject | T lymphocyte | - |
dc.subject | Coxsackievirus | - |
dc.subject | Myocarditis | - |
dc.title | Susceptibility to myocarditis is dependent on the response of αβ T lymphocytes to coxsackieviral infection | - |
dc.type | Article | - |
dc.description.nature | link_to_OA_fulltext | - |
dc.identifier.doi | 10.1161/01.RES.85.6.551 | - |
dc.identifier.pmid | 10488058 | - |
dc.identifier.scopus | eid_2-s2.0-0033578663 | - |
dc.identifier.volume | 85 | - |
dc.identifier.issue | 6 | - |
dc.identifier.spage | 551 | - |
dc.identifier.epage | 558 | - |
dc.identifier.isi | WOS:000082798600009 | - |
dc.identifier.issnl | 0009-7330 | - |