Resolution of plaque-type psoriasis: what is left behind (and reinitiates the disease).

Abstract

Psoriasis is a chronic inflammatory skin disease that involves numerous types of immune cells and cytokines resulting in an inflammatory feedback loop and hyperproliferation of the epidermis. A more detailed understanding of the underlying pathophysiology has revolutionized anti-psoriatic treatment and led to the development of various new drugs targeting key inflammatory cytokines such as IL-17A and IL-23. Successfully treated psoriatic lesions often resolve completely, leaving nothing visible to the naked eye. However, such lesions tend to recur within months at the exact same body sites. What is left behind at the cellular and molecular levels that potentially reinitiates psoriasis? Here, we elucidate the cellular and molecular "scar" and its imprints left after clinical resolution of psoriasis treated with anti-TNFα, anti-IL-17, or anti-IL-23 antibodies or phototherapy. Hidden cytokine stores and remaining tissue-resident memory T cells (TRMs) might hold the clue for disease recurrence.

• Authors: Theresa Benezeder, Peter Wolf
• Journal: Seminars in immunopathology (Semin Immunopathol) Vol. 41 Issue 6 Pg. 633-644 (11 2019) ISSN: 1863-2300 [Electronic] Germany
• PMID: 31673756 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)

Chemical References

• Biomarkers
• Cytokines
• Inflammation Mediators

Topics

• Biomarkers
• Cytokines (metabolism)
• Disease Management
• Disease Susceptibility
• Drug Development (methods)
• Epidermis (metabolism, pathology)
• Humans
• Inflammation Mediators (metabolism)
• Molecular Imprinting
• Molecular Targeted Therapy
• Psoriasis (diagnosis, etiology, metabolism, therapy)