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Abstract
Systemic lupus erythematosus (SLE) is an autoimmune disease that occurs primarily
in women (9:1 compared to men). Estrogen is a female sex hormone that acts on target
cells through specific receptor proteins and alters the rate of transcription of target
genes. Experiments in our laboratory have shown that calcineurin steady-state mRNA
levels and phosphatase activity increase when estrogen is cultured with SLE T cells.
This estrogen-dependent increase is dose-dependent, hormone-specific and temporally
regulated. Estrogen receptor antagonism by ICI 182,780 inhibits the increase in calcineurin
mRNA and phosphatase activity, while cycloheximide has no effect suggesting that new
protein synthesis is not required. Reverse transcription and polymerase chain amplification
indicate that estrogen receptor-alpha and estrogen-beta are expressed in human T cells.
However, calcineurin does not respond to estrogen stimulation in T cells from normal
females, males and lupus males. Taken together, these results indicate a differential
function of the estrogen receptor in women with lupus. A model is proposed that suggests
estrogen, acting through the estrogen receptor, enhances T cell activation in women
with lupus resulting in amplified T-B cells interactions, B cell activation and autoantibody
production.