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