Ilia J Elenkov
PMID: 15265778 DOI: 10.1196/annals.1321.010
Abstract
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.
Keywords: Corticotropin-Releasing Hormone / physiology
Cytokines / physiology
Glucocorticoids / pharmacology*
Histamine Release
Humans
Immune System Diseases / immunology
Infections / immunology
Mast Cells / immunology
Th1 Cells / drug effects*
Th1 Cells / immunology
Th2 Cells / drug effects*
Th2 Cells / immunology
Source: https://pubmed.ncbi.nlm.nih.gov/15265778/
Archive: https://archive.is/lcXgA
