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Cutaneous Glucocorticoidogenesis and Cortisol Signaling Are Defective in Psoriasis.

Abstract
Hannen et al. report that cutaneous glucocorticoidogenesis and expression of glucocorticoid receptors are inhibited in psoriatic skin. These findings substantiate the previous concept that deficient feedback of local proopiomelanocortin and glucocorticoids on cutaneous immunity contributes to inflammatory and autoimmune dermatoses. Restoration of efficient endogenous glucocorticoid signaling represents a realistic goal in treating psoriasis.
AuthorsAndrzej T Slominski, Anna A Brożyna, Robert C Tuckey
JournalThe Journal of investigative dermatology (J Invest Dermatol) Vol. 137 Issue 8 Pg. 1609-1611 (08 2017) ISSN: 1523-1747 [Electronic] United States
PMID28735612 (Publication Type: Journal Article, Review, Research Support, N.I.H., Extramural, Comment)
CopyrightCopyright © 2017 The Authors. Published by Elsevier Inc. All rights reserved.
Chemical References
  • Anti-Inflammatory Agents
  • Receptors, Glucocorticoid
  • Hydrocortisone
Topics
  • Administration, Cutaneous
  • Anti-Inflammatory Agents (administration & dosage, pharmacokinetics)
  • Humans
  • Hydrocortisone (administration & dosage, pharmacokinetics)
  • Psoriasis (drug therapy, metabolism, pathology)
  • Receptors, Glucocorticoid (metabolism)
  • Signal Transduction
  • Skin (drug effects, metabolism, pathology)

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