Abstract

Background: Vitiligo is an acquired chronic depigmenting disorder of the skin, characterized by the development of milky white macules and patches resulting from a selective loss of epidermal melanocytes. There are various theories about its pathogenesis and the etiology is multifactorial associating genetic and environmental factors together with metabolic and immune alterations. Objective: To demonstrate the role of circulating T regulatory cells (Treg) (specifically CD4+, CD4+25+, CD4+25+FoxP3) and serum level of IL-17 in pathogenesis ofnon-segmental vitiligo (NSV) in Egyptian patients. Patients and methods: This case-control study was carried out on eighty subjects in the period from January 2018 to March 2020, attending Dermatology, Andrology & STDs Outpatient Clinic of Mansoura University Hospital. Subjects were classified into two groups: Group (1): patients group included forty patients suffering from NSV (vitiligo patients group). Group (2): control group included forty persons who were selected from hospital workers with no personal or family history of vitiligo or systemic autoimmune diseases in their first-degree relatives. Results: After NBU-VB treatment, there was a highly statistically significant increase in CD4+%, CD4+25+% and CD4+25+FoxP3%expression with a mean of 12.1 ± 4 versus 10 ± 3.2, 3.5 ± 1.1 versus 3.2 ± 1 and 1.8 ± 0.6 versus 1.1 ± 0.3 when compared to before treatment levels respectively. Also, a highly statistically significant decrease in IL-17 level with the mean of 14.3 ± 4.1 versus 19.9 ± 6 pg/mL when compared to before treatment levels. There was a highly statistically significant positive correlation between CD4+25+% expression and CD4+% expression in vitiligo group before and after treatment. Conclusion: Lower CD4+%, CD4+25+% and CD4+25+FoxP3% expression and elevated serum levels of IL-17 positively were correlated with disease severity.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call