Glucocorticoids and the Th1/Th2 Balance

Jul 22, 2004Annals of the New York Academy of Sciences

Glucocorticoids and the balance between two types of immune responses

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Abstract

Increased levels of glucocorticoids may cause a selective suppression of Th1-cell immunity while promoting Th2-mediated immunity.

Glucocorticoids inhibit the production of pro-inflammatory cytokines such as interleukin-12 and tumor necrosis factor-alpha.
They upregulate the production of anti-inflammatory cytokines like interleukin-4, interleukin-10, and interleukin-13.
This mechanism could shift the immune response from a Th1-dominated profile to a Th2-dominated profile.
Increased glucocorticoid levels during stress may protect against excessive inflammation by mitigating Th1 responses.
Conditions that alter glucocorticoid levels may influence susceptibility to infections and the progression of autoimmune and allergic diseases.

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Evidence accumulated over the last 5-10 years indicates that glucocorticoids (GCs) inhibit the production of interleukin (IL)-12, interferon (IFN)-gamma, IFN-alpha, and tumor necrosis factor (TNF)-alpha 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.

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Glucocorticoids and the Th1/Th2 Balance

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