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The Journal of Immunology, Vol 158, Issue 12 5751-5756, Copyright © 1997 by American Association of Immunologists
ARTICLES |
S Poliak, F Mor, P Conlon, T Wong, N Ling, J Rivier, W Vale and L Steinman
Department of Immunology, Weizmann Institute of Science, Rehovot, Israel.
Corticotropin-releasing factor (CRF) exerts a major role in the stress response. Both CRF and urocortin, a newly discovered neuropeptide homologous to CRF, suppressed experimental autoimmune encephalomyelitis (EAE). Suppression of paralysis with CRF involved stimulation of the hypothalamic-pituitary-adrenal axis and inhibitory effects on an encephalitogenic T cell line. While CRF increased glucocorticoid production, which is known to block EAE, it also suppressed EAE in adrenalectomized rats, where glucocorticoid stimulation via CRF plays no role. Moreover, the encephalitogenicity of a T cell line exposed to CRF in vitro was reduced. Stress may influence autoimmune disease through the hypothalamic-pituitary-adrenal axis and directly via the immune system.
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