The hair follicle melanocytes in vitiligo in relation to disease duration

Anbar, Tag S.; Abdel-Raouf, Hamza; Awad, Sherif Shoukry; Ragaie, M H; Abdel‐Rahman, Amal T.

doi:10.1111/j.1468-3083.2009.03233.x

Cited by 43 publications

(49 citation statements)

References 10 publications

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“…Melanocytes in hair follicles seem to be more robust, so that normal hair colour often persists in the white patch [28]. Greying and eventual whitening of scalp and body hair in the condition of poliosis is not considered a form of vitiligo, but there may be some shared pathomechanisms; early greying of the hair can be seen in some vitiligo lesions [29]. New studies on the control of melanogenesis and constitutional skin colour point to roles for cytokines like SCF (stem cell factor), ET-1 (endothelin-1) and granulocyte macrophage colony stimulating factor [30].…”

Section: Melaninmentioning

confidence: 97%

“…Van den Boorn et al [218] expanded on all these findings in 2009: their study showed a prominent role for T-cells in vitiligo pathogenesis, being causative rather than just a consequence of other stimuli. Perilesional T-cells were easily identified in nine HLA-A2 + patients with progressive vitiligo, cultured and subjected to flow cytometric analysis using HLA-A2/peptide tetramers for tyrosinase-(369-377), gp100-(280-288), gp100-(209-217) and MART-1- (26)(27)(28)(29)(30)(31)(32)(33)(34)(35). A control antigen in the form of influenza virus-(58-66) was employed.…”

Section: Antigen-specific T-cellsmentioning

confidence: 99%

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Vitiligo, reactive oxygen species and T-cells

2010

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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.

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Section: Melaninmentioning

confidence: 97%

Section: Antigen-specific T-cellsmentioning

confidence: 99%

Vitiligo, reactive oxygen species and T-cells

2010

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“…While active melanocytes can be detected by DOPA and immunohistochemical staining (such as antibody NKI-beteb), amelanotic melanocytes can only be detected by the latter. [50,51] Ultrastructural studies have shown degenerative changes in early lesions. [52] Nevus depigmentosus can also present diagnostic challenges.…”

Section: Graft Versus Host Disease (Gvhd)mentioning

confidence: 98%

Invisible dermatoses

Mysore¹

2010

Indian J Dermatol Venereol Leprol

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'Invisible dermatoses' is a concept which has not received wide recognition, but is nevertheless very important both clinically and histologically. The term invisible dermatoses has been used in two contexts: a) Diseases, with out definite clinical features, and are therefore "invisible" to the clinician, but yet can be diagnosed by special investigations. b) Dermatoses which present with definite and obvious clinical features, but subtle or hidden histological features and are therefore "invisible" histologically. Diagnosis of such diseases represents a great challenge to both the dermatologist and dermatopathologist. This article discusses such diseases and offers clues and tools for their diagnosis. Diagnosis of such 'Invisible dermatoses' needs proper awareness, recognition of subtle features, special stains, special investigations such as immunofluorescence and histochemistry and proper clinicopathological correlation.

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“…Melanocytes are absent from 100% of white hairs. 115 ETIOLOGY Key points d The cause of vitiligo is unknown d The autoimmune hypothesis is the best supported theory d The neurohumoral, cytotoxic, and oxidative stress theories have moderate evidence d New theories focus on melanocytorrhagy and decreased melanocyte survival…”

Section: Associations and Syndromes Key Pointsmentioning

confidence: 99%