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Glucocorticoids and immune function.

Abstract
The prevailing notion has been that cytokines such as interleukin-1 released from sites of inflammation cross the blood-brain barrier and drive the hypothalamo-pituitary-adrenal (HPA) axis so that cortisol is released into the circulation to exert indiscriminate systemic anti-inflammatory effects. It is now clear that feedback from the HPA axis is subject to more subtle and localized regulation. The signal that activates cortisol release travels to the hypothalamus via vagal sensory afferents (so the brain 'knows' where the inflammation is), and the effects of the released cortisol are regulated within individual tissues via numerous mechanisms, including changes in the affinity of the cortisol receptors, and changes in the equilibrium point of the cortisol/cortisone shuttle (11 beta hydroxysteroid dehydrogenases 1 and 2). This equilibrium is locally regulated by cytokines. These mechanisms are central to the regulation of the balance of Th1 to Th2 cytokines within sites of inflammation, and to the appropriate or inappropriate termination of the inflammatory response in infections or autoimmunity.
AuthorsG A Rook
JournalBailliere's best practice & research. Clinical endocrinology & metabolism (Baillieres Best Pract Res Clin Endocrinol Metab) Vol. 13 Issue 4 Pg. 567-81 (Dec 1999) ISSN: 1532-1908 [Print] England
PMID10903815 (Publication Type: Journal Article, Review)
Chemical References
  • Glucocorticoids
  • Cortisone
  • Hydrocortisone
Topics
  • Cortisone (metabolism)
  • Glucocorticoids (physiology)
  • Humans
  • Hydrocortisone (metabolism)
  • Hypothalamo-Hypophyseal System (physiology)
  • Immune System (physiology)
  • Signal Transduction (physiology)
  • Stress, Physiological (immunology)
  • T-Lymphocytes (physiology)

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