Dysregulation of T Helper 17 Cell Pathway In Vitiligo.

BACKGROUND

Dysregulation of the T helper 17 (Th17) cell pathway can result in autoimmune activation and chronic inflammation. Vitiligo is an autoimmune disorder characterised by melanocyte cytotoxicity. The aim of this study was to examine the role of the Th17 pathway in the pathogenesis of vitiligo. The three components of the pathway were evaluated using plasma interleukin (IL6), IL23, and IL10 for the modulatory component, STAT3 and RORC gene expression for the mediator component, and plasma IL17A for the effector component.

METHOD: The study was carried out using a case-control design. The case group comprised patients diagnosed with vitiligo (n = 30), whereas the control group comprised healthy volunteers (n = 30). The plasma cytokine levels were measured by enzyme-linked immunosorbent assay. Gene expression in peripheral blood mononuclear cells was measured by real-time quantitative polymerase chain reaction.

RESULTS

In vitiligo patients, IL6 was 2.3 times higher (P < 0.001), IL23 was 1.1 times higher (P = 0.18), and IL10 was 2.5 times lower (P < 0.001). The fold change in the expression of the STAT3 gene was 2.27 times (P < 0.01) and that of the RORC gene was 3.8 times (P < 0.001) in vitiligo patients. Plasma IL17A was 1.6 times higher (P < 0.001) in vitiligo patients.

CONCLUSIONS

Together, these results indicate that the Th17 pathway is likely to be overactive in vitiligo due to dysregulation.