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Estradiol prevents and testosterone promotes Fas-dependent apoptosis in CD4+ Th2 cells by altering Bcl 2 expression.
Huber SA; Kupperman J; Newell MK; Department of Pathology, University of
December 30, 1999
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