Update on the pathogenesis of vitiligo
An. bras. dermatol
;
97(4): 478-490, July-Aug. 2022. tab, graf
Article
Dans Anglais
|
LILACS-Express
| LILACS
| ID: biblio-1383607
ABSTRACT
Abstract Vitiligo is a complex disease whose pathogenesis results from the interaction of genetic components, metabolic factors linked to cellular oxidative stress, melanocyte adhesion to the epithelium, and immunity (innate and adaptive), which culminate in aggression against melanocytes. In vitiligo, melanocytes are more sensitive to oxidative damage, leading to the increased expression of proinflammatory proteins such as HSP70. The lower expression of epithelial adhesion molecules, such as DDR1 and E-cadherin, facilitates damage to melanocytes and exposure of antigens that favor autoimmunity. Activation of the type 1-IFN pathway perpetuates the direct action of CD8+ cells against melanocytes, facilitated by regulatory T-cell dysfunction. The identification of several genes involved in these processes sets the stage for disease development and maintenance. However, the relationship of vitiligo with environmental factors, psychological stress, comorbidities, and the elements that define individual susceptibility to the disease are a challenge to the integration of theories related to its pathogenesis.
Texte intégral:
Disponible
Indice:
LILAS (Amériques)
Type d'étude:
Etude d'étiologie
/
Étude pronostique
langue:
Anglais
Texte intégral:
An. bras. dermatol
Thème du journal:
Dermatologie
Année:
2022
Type:
Article
Pays d'affiliation:
Brésil
/
Canada
Institution/Pays d'affiliation:
Hospital Irmandade Santa Casa de Misericórdia de Curitiba/BR
/
Mcgill University/CA
/
Pontifícia Universidade Católica do Paraná/BR
/
Universidade Estadual Paulista/BR
/
Universidade Estadual do Oeste do Paraná/BR
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