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Estradiol prevents and testosterone promotes Fas-dependent apoptosis in CD4+ Th2 cells by altering Bcl 2 expression.




 

Lupus. 1999;8(5):384-7. Unique Identifier : AIDSLINE MED/99394769

Coxsackievirus 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.

JOURNAL ARTICLE Animal Antigens, CD95/*PHYSIOLOGY Apoptosis/*DRUG EFFECTS Dose-Response Relationship, Drug Estradiol/*PHARMACOLOGY Female Male Mice Proto-Oncogene Proteins c-bcl-2/*ANALYSIS Rabbits Support, Non-U.S. Gov't Support, U.S. Gov't, P.H.S. Testosterone/*PHARMACOLOGY Th1 Cells/DRUG EFFECTS/PHYSIOLOGY Th2 Cells/*DRUG EFFECTS/PHYSIOLOGY 3T3 Cells



 




Information in this article was accurate in December 30, 1999. The state of the art may have changed since the publication date. This material is designed to support, not replace, the relationship that exists between you and your doctor. Always discuss treatment options with a doctor who specializes in treating HIV.