| Vitiligo, reactive oxygen species and T-cells. | |
| | |
MedLine Citation:
|
PMID: 20958268 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
|
The acquired depigmenting disorder of vitiligo affects an estimated 1% of the world population and constitutes one of the commonest dermatoses. Although essentially asymptomatic, the psychosocial impact of vitiligo can be severe. The cause of vitiligo remains enigmatic, hampering efforts at successful therapy. The underlying pathogenesis of the pigment loss has, however, been clarified to some extent in recent years, offering the prospect of effective treatment, accurate prognosis and rational preventative strategies. Vitiligo occurs when functioning melanocytes disappear from the epidermis. A single dominant pathway is unlikely to account for all cases of melanocyte loss in vitiligo; rather, it is the result of complex interactions of biochemical, environmental and immunological events, in a permissive genetic milieu. ROS (reactive oxygen species) and H2O2 in excess can damage biological processes, and this situation has been documented in active vitiligo skin. Tyrosinase activity is impaired by excess H2O2 through oxidation of methionine residues in this key melanogenic enzyme. Mechanisms for repairing this oxidant damage are also damaged by H2O2, compounding the effect. Numerous proteins and peptides, in addition to tyrosinase, are similarly affected. It is possible that oxidant stress is the principal cause of vitiligo. However, there is also ample evidence of immunological phenomena in vitiligo, particularly in established chronic and progressive disease. Both innate and adaptive arms of the immune system are involved, with a dominant role for T-cells. Sensitized CD8+ T-cells are targeted to melanocyte differentiation antigens and destroy melanocytes either as the primary event in vitiligo or as a secondary promotive consequence. There is speculation on the interplay, if any, between ROS and the immune system in the pathogenesis of vitiligo. The present review focuses on the scientific evidence linking alterations in ROS and/or T-cells to vitiligo. |
| | |
Authors:
|
Steven J Glassman |
Related Documents
:
|
8609398 - Cytokines suppress apoptosis independent of increases in reactive oxygen levels. 20689558 - Bid-mediated mitochondrial damage is a key mechanism in glutamate-induced oxidative str... 19356708 - Oxidative preconditioning promotes bone marrow mesenchymal stem cells migration and pre... 20969948 - Specific activation of human neutrophils by scorpion venom: a flow cytometry assessment. 10447398 - T cell signaling: a decision of life and death. 9300088 - Fluorometric and colorimetric detection of caspase activity associated with apoptosis. |
Publication Detail:
|
Type: Journal Article; Review |
Journal Detail:
|
Title: Clinical science (London, England : 1979) Volume: 120 ISSN: 1470-8736 ISO Abbreviation: Clin. Sci. Publication Date: 2011 Feb |
Date Detail:
|
Created Date: 2010-10-20 Completed Date: 2011-01-03 Revised Date: - |
Medline Journal Info:
|
Nlm Unique ID: 7905731 Medline TA: Clin Sci (Lond) Country: England |
Other Details:
|
Languages: eng Pagination: 99-120 Citation Subset: IM |
Affiliation:
|
Division of Dermatology, Department of Medicine, University of Ottawa, Ottawa, Ontario, Canada. sglassman@toh.on.ca |
Export Citation:
|
APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
|
Antioxidants
/
metabolism Autoimmunity Humans Hydrogen Peroxide / metabolism Melanins / physiology Melanocytes / pathology Reactive Oxygen Species / metabolism* T-Lymphocyte Subsets / immunology* Vitiligo / immunology*, pathology |
| Chemical | |
Reg. No./Substance:
|
0/Antioxidants; 0/Melanins; 0/Reactive Oxygen Species; 7722-84-1/Hydrogen Peroxide |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
Previous Document: Phosphate toxicity: new insights into an old problem.
Next Document: CXCL8 enhances the angiogenic activity of umbilical cord blood-derived outgrowth endothelial cells i...