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Vitiligo pp 285-301 | Cite as

Immunity/Immunopathology

  • Kirsten C. Webb
  • Steven W. Henning
  • I. Caroline Le PooleEmail author
Chapter

Abstract

For appreciable time, the pathophysiology leading to ultimate melanocyte destruction remained uncertain. This is because skin-infiltrating T cells involved in melanocyte loss are few in number and are only observed in actively depigmenting skin; thus, such infiltrates are easily overlooked. Moreover, T cells were more difficult to distinguish before antibodies became readily available for immunohistology. Ample support exists for autoimmunity as a chief etiopathological factor in vitiligo: susceptible individuals exhibit polymorphisms in immune regulatory genes which promote autoimmunity in the cutaneous microenvironment; additionally, vitiligo has a well-established association with other autoimmune diseases. Among the possibly involved cell populations, Langerhans cells might contribute to depigmentation on-site (perhaps through continued melanocyte antigen presentation to cytotoxic T cells), thereby preventing viability of any melanocytes attempting to repopulate the skin. The HSP-native protein complexes can trigger a local immune response directed at the cells from which the native proteins originate. Upon melanocyte stress and subsequent HSP70i release, antigen-presenting cells will recruit an initial cohort of melanocyte-reactive T cells that produce IFN-γ upon antigen recognition. This would lead to CXCL10 production and further recruitment to the epidermis. The absence of Tregs in vitiligo skin is likewise best explained by differential chemokine expression in lesional skin, mainly involving CCL22.

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Copyright information

© Springer Nature Switzerland AG 2019

Authors and Affiliations

  • Kirsten C. Webb
    • 1
  • Steven W. Henning
    • 2
  • I. Caroline Le Poole
    • 3
    Email author
  1. 1.Division of Dermatology, Department of MedicineLoyola University ChicagoMaywoodUSA
  2. 2.Lurie Comprehensive Cancer CenterNorthwestern UniversityChicagoUSA
  3. 3.Professor of Dermatology, Microbiology and ImmunologyNorthwestern University at ChicagoILUSA

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