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Steroid Hormones and the T-Cell Cytokine Profile (Paperback, Softcover reprint of the original 1st ed. 1997)
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Steroid Hormones and the T-Cell Cytokine Profile (Paperback, Softcover reprint of the original 1st ed. 1997)
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The fact that certain adrenal steroid hormones are
immunosuppressive and anti-inflammatory has been known for many
years, and is routinely exploited by physicians. These effects are
attributable to glucocorticoid steroids such as cortisol.
Pharmacological doses of glucocorticoids inhibit most or all T cell
types. However we now know that the effect of exposure to raised
physiological levels is mainly to drive developing lymphocyte
responses towards a Th2 cytokine profile (interleukin-4 secreting)
while suppressing the development ofThi (gamma interferon-
secreting) lymphocytes. Only recently have two further regulatory
mechanisms become appar- ent. First, these effects of cortisol are
balanced by pro-inflammatory and ThI-enhancing effects of another
adrenal steroid, dehydroepiandro- sterone sulfate (DHEAS). Second,
the activity of cortisol is directly modulated by enzymes in the
target organs and lymphoid tissues that convert it into inactive
cortisone. This new information leads to the possibility that
immunoregulatory steroids could be used by physicians in novel
ways. We can envisage steroid combinations that exploit the
anti-inflammatory effects of corti- sol, while the Thi-suppressing
and Th2-promoting properties of these hormones are opposed by
derivatives of DHEAS. Such therapies are already proving effective
in animal models of infection, and could revol- utionize treatment
of Th2-mediated diseases such as asthma, where the
anti-inflammatory effects of cortisol are desirable but the effects
on T lymphocyte differentiation are not.
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