The role of helper and regulatory T cells in the pathogenesis of vitiligo

BackgroundAlterations in cellular immunity, including CD4+ T and CD8+ T lymphocytes, have been proposed in the pathogenesis of vitiligo. There is also a proposed role for cytokines in the depigmentation observed in vitiligo. However, previous reports on the role of cytokines in the pathogenesis of vitiligo have been few in number.ObjectiveThe purpose of this investigation was to assess the role of the major cytokines produced by T-helper 1 and 2 cells as well as T-helper 17 and regulatory T cells in the pathogenesis of vitiligo.MethodsForty patients with vitiligo and 40 age- and sex-matched healthy control subjects were enrolled in the study. Serum interleukin (IL)-4, IL-6, IL-10, IL-17, interferon-γ, tumor necrosis factor-β, and transforming growth factor-β levels were detected by enzyme-linked immunosorbent assay in both groups. The correlations of serum cytokine levels with age of onset, sex, duration of disease, type and activity of vitiligo, percentage of involved body area, Koebner positivity, family history, and the presence of associated autoimmune diseases were assessed.ResultsSerum transforming growth factor-β levels were significantly decreased in the vitiligo group compared with the control group (P = .004). No difference was detected between the patient and control groups in mean levels of serum IL-6, IL-10, and tumor necrosis factor-β. In the patients with vitiligo, serum IL-17 levels were positively correlated with the extent of body area involvement (rho = 0.329, P = .038).LimitationsTissue cytokines compared with those in the peripheral blood were not measured.ConclusionAlthough multiple factors have been implicated in the pathogenesis of vitiligo, reduced serum transforming growth factor-β levels, as observed in patients in the current investigation, may contribute to enhanced cellular immunity. This may facilitate the occurrence of vitiligo by leading to diminished maturation of regulatory T cells, followed by impaired inhibition of inflammation.