Abstract

BackgroundVitiligo is a common skin disorder, characterized by progressive skin de-pigmentation due to the loss of cutaneous melanocytes. The exact cause of melanocyte loss remains unclear, but a large number of observations have pointed to the important role of cellular immunity in vitiligo pathogenesis.Methodology/Principal FindingsIn this study, we characterized T cell and inflammation-related dermal dendritic cell (DC) subsets in pigmented non-lesional, leading edge and depigmented lesional vitiligo skin. By immunohistochemistry staining, we observed enhanced populations of CD11c+ myeloid dermal DCs and CD207+ Langerhans cells in leading edge vitiligo biopsies. DC-LAMP+ and CD1c+ sub-populations of dermal DCs expanded significantly in leading edge and lesional vitiligo skin. We also detected elevated tissue mRNA levels of IL-17A in leading edge skin biopsies of vitiligo patients, as well as IL-17A positive T cells by immunohistochemistry and immunofluorescence. Langerhans cells with activated inflammasomes were also noted in lesional vitiligo skin, along with increased IL-1ß mRNA, which suggest the potential of Langerhans cells to drive Th17 activation in vitiligo.Conclusions/SignificanceThese studies provided direct tissue evidence that implicates active Th17 cells in vitiligo skin lesions. We characterized new cellular immune elements, in the active margins of vitiligo lesions (e.g. populations of epidermal and dermal dendritic cells subsets), which could potentially drive the inflammatory responses.

Highlights

  • Vitiligo is a common skin disorder, affecting over 0.5% of the world population [1]

  • Infiltrating T cells have been found in peri-lesional vitiligo skin, and circulating auto-antibodies and auto-reactive CD8+ cytotoxic T cells that recognize melanocyte antigens were detected in the sera of a high proportion of vitiligo patients [39]

  • T cells expanded from peri-lesional vitiligo skin show a predominately type 1 cytokine profile (i.e. IFN-c and TNF-a) [12]

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Summary

Introduction

Vitiligo is a common skin disorder, affecting over 0.5% of the world population [1]. It is characterized by progressive skin depigmentation due to the loss of cutaneous melanocytes and abnormal melanocyte function. The exact cause of melanocyte loss in nonsegmental vitiligo is still debatable, but many observations have pointed to the important role of cellular immunity in its disease pathogenesis. Vitiligo is a common skin disorder, characterized by progressive skin de-pigmentation due to the loss of cutaneous melanocytes. The exact cause of melanocyte loss remains unclear, but a large number of observations have pointed to the important role of cellular immunity in vitiligo pathogenesis

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