Although lupus affects prepubertal males and females equally, during puberty it manifests a striking preference for females that is maintained throughout the reproductive years. Thus, female hormonal factors play a permissive role at least, whereas male hormonal factors play a protective one in the expression of SLE. This has been further supported by studies in murine strains in which it has been clearly shown that estrogens have deleterious effects on lupus-prone experimental animals, whereas androgens are protective.

Estrogens act on target cells after binding to their cytoplasmic estrogen receptors, which belong to the group of nuclear receptors. The estrogen-estrogen receptor complex acquires transcription factor activity, and, after entrance into the nucleus and binding to specific estrogen-response elements found in the promoters of several genes, it modulates their transcription. Estrogen receptors are located in the cytoplasm and on the cell surface membrane. In murine T cells, membrane estrogen receptors, on binding to estradiol, mediate a rise in the concentration of intracellular calcium, which is a pivotal second messenger. Estrogen response elements are found in the promoters of the proto-oncogenes c-fos and c-jun and affect their transcription and, therefore, the levels of the transcription factor AP-1, which is a fos/jun hetero-dimer. Estrogens cause a significant increase in the amounts of calcineurin transcripts and also in calcineurin phosphatase activity in SLE T cells. The latter finding may provide a molecular explanation for the role of estrogens in autoimmunity (Tsokos and Boumpas 2002).

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