Hostname: page-component-cd9895bd7-7cvxr Total loading time: 0 Render date: 2024-12-18T08:25:54.377Z Has data issue: false hasContentIssue false

Immunological pathomechanisms in vitiligo

Published online by Cambridge University Press:  12 February 2004

E. Helen Kemp
Affiliation:
Division of Clinical Sciences, Northern General Hospital, University of Sheffield, Sheffield, S5 7AU, UK.
Elizabeth A. Waterman
Affiliation:
Division of Clinical Sciences, Northern General Hospital, University of Sheffield, Sheffield, S5 7AU, UK.
Anthony P. Weetman
Affiliation:
Division of Clinical Sciences, Northern General Hospital, University of Sheffield, Sheffield, S5 7AU, UK.

Abstract

Vitiligo is a depigmenting disorder characterised by the loss of melanocytes from the cutaneous epidermis. Although the exact aetiology of vitiligo has not yet been established, the abnormal immune responses frequently observed in vitiligo patients have led to the suggestion that, in some cases, the condition has an autoimmune component. Briefly, circulating autoantibodies and autoreactive T cells that recognise pigment cell antigens have been detected in the sera of a significant proportion of vitiligo patients compared with healthy individuals. In addition, vitiligo is often associated with other disorders that have an autoimmune origin, including Hashimoto's thyroiditis, Graves' disease, type 1 insulin-dependent diabetes mellitus and Addison's disease. Furthermore, effective use of immunosuppressive therapies to treat vitiligo, the association of vitiligo with certain major histocompatibility complex antigens, and evidence from animal models of the disease have all added credence to the hypothesis that immune reactions play a role in vitiligo pathogenesis. This review presents and discusses the evidence for immunological pathomechanisms in vitiligo.

Type
Review Article
Copyright
© Cambridge University Press 2001

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)