Vitiligo vulgaris (VV) and psoriasis vulgaris (PV) are common dermatoses, with a worldwide occurrence of 0.5-1% and 1-3%, respectively. An imbalance between effector T cells and regulatory T cells (Tregs) can result in the pathogenesis of cutaneous immune diseases. In VV, interleukin (IL)-17-producing T-helper (Th) 17 cells are increased in the lesional skin as seen in PV (1). However, the number of Tregs is drastically reduced in the lesional skin of VV, which may allow an activation of effector T cells (2). In PV, an increased number of lesional Tregs was indicated (3, 4). While both lesional Th17 cells and Tregs are increased in PV, the ratio of Th17 cells to Tregs was shown to be inversely correlated with the psoriasis area and severity index (PASI). It has recently been proposed that Tregs readily turn into Th17 cells in PV, which potentially perpetuates the inflammatory process that characterises the disease (5). Herein, we present a case with the coexistent skin lesions of VV and PV with immunohistochemical analyses.
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Ono et al. (2014) studied this question.
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