Abstract
Vitiligo (VIT) is caused by loss and degradation of functional epidermal melanocytes. Studies have indicated that melanocyte destruction may be associated with an imbalance between regulatory T cells (Treg cells) and effector T cells (Teff cells). The current study aimed to investigate the molecular mechanism through which Treg/Teff balance affects VIT pathogenesis. To explore this, peripheral blood mononuclear cells were isolated from patients with VIT and healthy individuals. The present study revealed that the proportions of CD4+ T cells, Treg cells and T helper 1 (Th1) cells were decreased in patients with VIT, but those of Teff cells (Th17 and Th22 cells) were increased; additionally, Foxp3 expression was decreased, but the expression levels of interferon‑γ, interleukin (IL)‑17A and IL‑22 were increased. Furthermore, in patients with VIT, microRNA (miR)‑21‑5p expression was decreased, while that of STAT3 was increased. Further <em>in vitro</em> experiments in CD4+ T cells revealed that STAT3 was targeted by miR‑21‑5p. Functional analysis further indicated that miR‑21‑5p overexpression in Th17‑polarized CD4+ T cells decreased the proportion of Teff cells and associated cytokines, such as IL‑17A and IL‑22, but increased the proportion of Treg cells and Foxp3. However, the effects of miR‑21‑5p overexpression were partly reversed by STAT3 overexpression. Increased apoptosis of melanocytes was detected after co‑culture with Th17‑polarized CD4+ T cells in the presence of a miR‑21‑5p mimic. However, this indirect effect of the miR‑21‑5p mimic on melanocytes was decreased via STAT3 overexpression. Therefore, miR‑21‑5p may protect melanocytes via targeting STAT3 and regulating Treg/Teff balance. The current findings may provide a possible treatment method for managing VIT.