Narrow band ultraviolet B therapy deactivates Th1/Th17 pathway and activates Th2 cytokines secretion in Egyptian psoriatic arthritis patients

  • Farid A
  • Tawfik A
  • Elsioufy B
  • et al.
N/ACitations
Citations of this article
13Readers
Mendeley users who have this article in their library.

This article is free to access.

Abstract

ABSTRACT Psoriasis is a chronic autoimmune disorder that affects 3-4% of the world population. Keratinocytes and immune cells in patient’s skin secrets excess pro-inflammatory cytokines that in turn activates the differentiation of T helper cells (Th) into Th1 and Th17 and deactivates Th2 pathway. Several phototherapies have been used in treatment of moderate and severe psoriatic patients; among them narrowband ultraviolet B (NB-UVB, 311 nm) is the most effective. We aims to evaluate the therapeutic effect of NB-UVB exposure in 80 Egyptian plaque psoriatic patients with and without psoriasis arthritis development. This will be accomplished by measuring serum cytokines levels (IL-10, -12, -17, -23 and -34) and high sensitive C reactive protein before and after treatment. A significant elevation in Th2 pathway cytokine, IL-10, and significant decrease in Th1/Th17 pathway cytokines were observed after treatment. This indicates the success of NB-UVB therapy in down modulating IL-12 and IL-23/Th17 axis. The pathological conditions in psoriatic arthritis patients were improved by NB-UVB targeted to the skin. As serum cytokines levels in these patients indicated that the reduction in Th1/Th17 inflammatory cytokines and elevation of Th2 anti-inflammatory cytokines was not restricted to skin lesions only, but also, spread in patients’ body and improve their pathologic.

Cite

CITATION STYLE

APA

Farid, A., Tawfik, A., Elsioufy, B., & Safwat, G. (2020). Narrow band ultraviolet B therapy deactivates Th1/Th17 pathway and activates Th2 cytokines secretion in Egyptian psoriatic arthritis patients. Journal of Radiation Research and Applied Sciences, 13(1), 356–361. https://doi.org/10.1080/16878507.2020.1742443

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free