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Production and Reduces the Severity of Experimental Autoimmune Encephalomyelitis in Cytokine Knockout Mice1
,
*
Department of Neurology and
Neurological Sciences Institute, Oregon Health Sciences University, and
Neuroimmunology Research, Department of Veterans Affairs, Portland, OR 97201
A shift toward Th2 cytokine production has been demonstrated during
pregnancy and high dose estrogen therapy and is thought to be the
primary mechanism by which estrogen suppresses the development of
experimental autoimmune encephalomyelitis. However, low dose estrogen
treatment is equally protective in the absence of a significant shift
in cytokine production. In this study cytokine-deficient mice were
treated with estrogen to determine whether a shift in Th2 cytokine
production was required for the protective effects of hormone therapy.
Estrogen effectively suppressed the development of experimental
autoimmune encephalomyelitis in IL-4 and IL-10 knockout mice and in
wild type littermate mice with a similar potency of protection.
Significant disease suppression was also seen in IFN-
-deficient
mice. The decrease in disease severity was accompanied by a concomitant
reduction in the number of proinflammatory cytokine- and
chemokine-producing cells in the CNS. Although there was no apparent
increase in compensatory Th2 cytokine production in cytokine-deficient
mice, there was a profound decrease in the frequency of
TNF-
-producing cells in the CNS and the periphery. Therefore, we
propose that one mechanism by which estrogen protects females from the
development of cell-mediated autoimmunity is through a
hormone-dependent regulation of TNF-
production.
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