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Glucocorticoids and the Th1/Th2 Balance
ILIA J. ELENKOV
Clinical Neuroendocrinology Branch, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 20892, USA
Address correspondence to: Dr. Ilia J. Elenkov, Clinical Neuroendocrinology Branch, National Institute of Mental Health, National Institutes of Health, Building 10, Room 2D46, 10 Center Drive, Bethesda, MD 20892. Elenkovi{at}mail.nih.gov
Ann. N.Y. Acad. Sci. 1024: 138-146 (2004).
Evidence accumulated over the last 5-10 years indicates that glucocorticoids (GCs) inhibit the production of interleukin (IL)-12, interferon (IFN)-  , IFN-  , and tumor necrosis factor (TNF)- by antigen-presenting cells (APCs) and T helper (Th)1 cells, but upregulate the production of IL-4, IL-10, and IL-13 by Th2 cells. Through this mechanism increased levels of GCs may systemically cause a selective suppression of the Th1-cellular immunity axis, and a shift toward Th2-mediated humoral immunity, rather than generalized immunosuppression. During an immune response and inflammation, the activation of the stress system, and thus increased levels of systemic GCs through induction of a Th2 shift, may actually protect the organism from systemic "overshooting" with Th1/pro-inflammatory cytokines and other products of activated macrophages with tissue-damaging potential. However, conditions associated with significant changes of GCs levels, such as acute or chronic stress or cessation of chronic stress, severe exercise, and pregnancy and postpartum, through modulation of the Th1/Th2 balance may affect the susceptibility to or the course of infections as well as autoimmune and atopic/allergic diseases.
Key Words: glucocorticoids • stress • interleukin-12 • interleukin-10 • Th1 cells • Th2 cells • autoimmunity • allergy • inflammation • rheumatoid arthritis • multiple sclerosis
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