Linked Life Data

10455518

Source:http://linkedlifedata.com/resource/pubmed/id/10455518

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SubjectPredicateObjectContext
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pubmed-article:10455518pubmed:abstractTextCoxsackievirus B3 (CVB3) induces myocarditis in male BALB/c mice. Female mice are resistant to viral myocarditis, except in the third trimester of pregnancy and postpartum. Cardiac damage is mediated by T lymphocytes activated during virus infection. Th1 (interferon-gamma+) cell responses promote cardiac injury, while disease resistance correlates to preferential activation of Th2 (interleukin-4+) cell responses. CVB3-specific Th1 and Th2 cell clones were established, treated with between 0 and 100 ng/ml 17beta estradiol and 4-androsten-17beta-ol-one (testosterone) for two days, 51Cr-labeled and cultured on FasL-transfected 3T3 cells to determine susceptibility to Fas-dependent apoptosis. Testosterone treatment enhanced Th2 cell lysis while estradiol treatment was protective. Staining of Th2 cells for Bcl 2, an anti-apoptotic factor, indicates that Bcl 2 expression increased in these cells with estradiol but decreased with testosterone exposure. Hormone-induced changes in Bcl 2 expression likely explain the selective survival of Th2 cells in females and prevention of viral myocarditis.lld:pubmed
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pubmed-article:10455518pubmed:dateRevised2007-11-14lld:pubmed
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pubmed-article:10455518pubmed:articleTitleEstradiol prevents and testosterone promotes Fas-dependent apoptosis in CD4+ Th2 cells by altering Bcl 2 expression.lld:pubmed
pubmed-article:10455518pubmed:affiliationDepartment of Pathology, University of Vermont, Burlington 05405, USA.lld:pubmed
pubmed-article:10455518pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:10455518pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
pubmed-article:10455518pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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