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

Department of Pathology, University of Vermont, Burlington, VT 05405, USA

J Kupperman

M K Newell

Department of Pathology, University of Vermont, Burlington, VT, USA

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 17ß estradiol and 4-androsten-17ß-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.

Key Words: estradiol • testosterone • myocarditis • apoptosis

Lupus, Vol. 8, No. 5, 384-387 (1999)
DOI: 10.1177/096120339900800511


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