PROFILE OF TH17 PATHWAY IN THE PATHOGENESIS OF VITILIGO

Abstract

Background: Vitiligo is caused by a confluence of hereditary predispositions and environmental stimuli. Its etiology is yet unknown, though. Recent research suggests that cell-mediated cytotoxicity, oxidative stress, neurohumoral factors, and autoimmunity are all involved in the pathophysiology of vitiligo. According to the autoimmune theory, the continuous production of autoantibodies and the significant infiltration of cytotoxic (CD8+) T-cells at the site of inflammation in the skin region result in the targeted killing of melanocytes.

Material and Method: This study was conducted in the Dept. of Dermatology. This is a case–control study. Clinically diagnosed vitiligo patients were grouped as cases while healthy volunteers were grouped as controls. Both the groups comprised age and gender-matched individuals. Whole blood samples collected from both groups were used to estimate the selected cytokines (IL6, IL23, IL10, and IL17) level.

Result: The clinical and demographic details of the study participants are summarised in Table 1. The majority of the patients showed the non-segmental type of vitiligo (86.7%). Some patients (10%) reported a familial history of vitiligo.

Conclusion: The plasma's cytokine concentrations were examined. In vitiligo, IL6 and IL17 plasma levels were 2.3 and 1.6 times higher, respectively, than in controls. In contrast, vitiligo patients had 2.5-fold lower plasma levels of the suppressor cytokine (IL10). Plasma IL23 levels did not significantly differ between the groups, though. In addition, vitiligo patients had larger ratios of inducers to suppressors (IL6/IL10 and IL23/IL10) than controls. These findings suggested that the cytokine profile in vitiligo is proinflammatory.

Keywords: IL6, IL23, TH17, Vitiligo and Autoimmune