Estrogens are believed to play a role in the etiology of both human and mur
ine systemic lupus erythematosus (lupus; SLE), presumably through the agenc
y of their cellular receptor proteins. There is now considerable interest i
n the molecular mechanism of action of estrogens in immune tissues, particu
larly with regard to autoimmune disorders, which are generally more prevale
nt in women. In this laboratory, an attempt is being made to characterize e
strogen receptors in murine models of SLE and to try and relate this to est
rogen receptor function in vivo. The initial aim was to compare binding pro
perties of estrogen receptors in brain, reproductive and immune tissues of
BALB/c and MRL/MP-lpr/lpr mice. The latter strain spontaneously develops an
autoimmune disease resembling human systemic lupus erythematosus (lupus; S
LE). It is hypothesized that estradiol, through its receptors, mediates the
progression of murine SLE, and that in autoimmune disease, the estrogen re
ceptor is functionally and/or structurally changed. Initial studies suggest
that there are differences in estrogen receptors between BALB/c mice, whic
h do not get autoimmune disease, and two strains that do, MRL/MP-lpr/lpr an
d NZB/W mice. In MRL mice, these differences may be reflected in impaired p
riming of the progesterone receptor. (C) 2001 Elsevier Science B.V. All rig
hts reserved.