title: Th17 cells and activated dendritic cells are increased in vitiligo lesions.
abstract: BACKGROUND
  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.
  
  
  RESULTS
  In 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
  These 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.
authors.affiliation: Laboratory for Investigative Dermatology, The Rockefeller University, New York, New York, United States of America.
authors.forename: Claire Q F
authors.initials: CQ
authors.lastname: Wang
authors.forename: Andres E
authors.initials: AE
authors.lastname: Cruz-Inigo
authors.forename: Judilyn
authors.initials: J
authors.lastname: Fuentes-Duculan
authors.forename: Dariush
authors.initials: D
authors.lastname: Moussai
authors.forename: Nicholas
authors.initials: N
authors.lastname: Gulati
authors.forename: Mary
authors.initials: M
authors.lastname: Sullivan-Whalen
authors.forename: Patricia
authors.initials: P
authors.lastname: Gilleaudeau
authors.forename: Jules A
authors.initials: JA
authors.lastname: Cohen
authors.forename: James G
authors.initials: JG
authors.lastname: Krueger
mesh_terms: D048868:Adaptor Proteins, Signal Transducing / Q000378:metabolism; D051017:Apoptosis Regulatory Proteins / Q000378:metabolism; D001706:Biopsy; D002452:Cell Count; D002454:Cell Differentiation / Q000276:immunology; D003713:Dendritic Cells / Q000276:immunology* / Q000473:pathology*; D020405:Dermis / Q000276:immunology / Q000473:pathology; D006801:Humans; D020381:Interleukin-17 / Q000276:immunology; D007801:Langerhans Cells / Q000276:immunology / Q000473:pathology; D008213:Lymphocyte Activation / Q000276:immunology; D008544:Melanocytes / Q000473:pathology; D000070576:NLR Proteins; D018417:Th1 Cells / Q000276:immunology / Q000473:pathology; D058504:Th17 Cells / Q000276:immunology*; D018418:Th2 Cells / Q000276:immunology / Q000473:pathology; D014820:Vitiligo / Q000276:immunology* / Q000473:pathology*
chemical_list: D048868:Adaptor Proteins, Signal Transducing; D051017:Apoptosis Regulatory Proteins; D020381:Interleukin-17; D000070576:NLR Proteins; C427903:NLRP1 protein, human