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Departments of
*
Neurology,
Molecular Microbiology and Immunology, and
Cell and Neurobiology, University of Southern California School of Medicine, Los Angeles, CA 90033
Steroid hormones have long been known to modulate immune function,
and recent studies indicate that one of the means by which they do so
involves effects on the secretion of immunoregulatory cytokines. Our
laboratory has found recently that estradiol (E2) selectively modifies
cytokine secretion in proteolipid protein (PLP)-specific,
CD4+ T cell clones isolated from patients with the
demyelinating disease, multiple sclerosis, and from normal control
subjects. The data suggest that E2 may play a role in regulating the
balance between pro- and antiinflammatory conditions, especially at
concentrations typical of pregnancy. To determine whether other
pregnancy-associated steroid hormones are capable of similar activity,
we expanded our testing to include estrone (E1), estriol (E3),
progesterone, and dexamethasone. The results indicate that E1 and E3
enhance secretion of Ag- or anti-CD3-stimulated IL-10 and IFN-
in dose-dependent fashion, almost identical to that of E2. The effect
on IL-10 was more potent than occurred with IFN-. In addition, E1
and E3, like E2, had a biphasic effect on TNF-
ß secretion, with
low concentrations stimulatory, and high doses inhibitory. None of the
estrogens influenced IL-4 or TGF-ß secretion. Progesterone enhanced
secretion of IL-4, without affecting any other tested cytokine.
Finally, dexamethasone induced TGF-ß secretion, but inhibited IFN-
and TNF-ß. This differential effect of steroid hormones on the
secretion of cytokines by CD4+ human T cell clones is
consistent with the possibility that, collectively, they promote
antiinflammatory conditions at high concentrations typical of
pregnancy.
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