Update on the pathogenesis of vitiligo
Autor(a) principal: | |
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Data de Publicação: | 2022 |
Outros Autores: | , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Anais brasileiros de dermatologia (Online) |
Texto Completo: | http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0365-05962022000400478 |
Resumo: | 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. |
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Update on the pathogenesis of vitiligoAutoimmunityOxidative stressPigmentationVitiligoAbstract 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.Sociedade Brasileira de Dermatologia2022-08-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersiontext/htmlhttp://old.scielo.br/scielo.php?script=sci_arttext&pid=S0365-05962022000400478Anais Brasileiros de Dermatologia v.97 n.4 2022reponame:Anais brasileiros de dermatologia (Online)instname:Sociedade Brasileira de Dermatologia (SBD)instacron:SBD10.1016/j.abd.2021.09.008info:eu-repo/semantics/openAccessMarchioro,Helena ZenedinCastro,Caio César Silva deFava,Vinicius MedeirosSakiyama,Paula HitomiDellatorre,GersonMiot,Hélio Amanteeng2022-07-25T00:00:00Zoai:scielo:S0365-05962022000400478Revistahttp://www.anaisdedermatologia.org.br/https://old.scielo.br/oai/scielo-oai.phpabd@sbd.org.br||revista@sbd.org.br1806-48410365-0596opendoar:2022-07-25T00:00Anais brasileiros de dermatologia (Online) - Sociedade Brasileira de Dermatologia (SBD)false |
dc.title.none.fl_str_mv |
Update on the pathogenesis of vitiligo |
title |
Update on the pathogenesis of vitiligo |
spellingShingle |
Update on the pathogenesis of vitiligo Marchioro,Helena Zenedin Autoimmunity Oxidative stress Pigmentation Vitiligo |
title_short |
Update on the pathogenesis of vitiligo |
title_full |
Update on the pathogenesis of vitiligo |
title_fullStr |
Update on the pathogenesis of vitiligo |
title_full_unstemmed |
Update on the pathogenesis of vitiligo |
title_sort |
Update on the pathogenesis of vitiligo |
author |
Marchioro,Helena Zenedin |
author_facet |
Marchioro,Helena Zenedin Castro,Caio César Silva de Fava,Vinicius Medeiros Sakiyama,Paula Hitomi Dellatorre,Gerson Miot,Hélio Amante |
author_role |
author |
author2 |
Castro,Caio César Silva de Fava,Vinicius Medeiros Sakiyama,Paula Hitomi Dellatorre,Gerson Miot,Hélio Amante |
author2_role |
author author author author author |
dc.contributor.author.fl_str_mv |
Marchioro,Helena Zenedin Castro,Caio César Silva de Fava,Vinicius Medeiros Sakiyama,Paula Hitomi Dellatorre,Gerson Miot,Hélio Amante |
dc.subject.por.fl_str_mv |
Autoimmunity Oxidative stress Pigmentation Vitiligo |
topic |
Autoimmunity Oxidative stress Pigmentation Vitiligo |
description |
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. |
publishDate |
2022 |
dc.date.none.fl_str_mv |
2022-08-01 |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0365-05962022000400478 |
url |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0365-05962022000400478 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
10.1016/j.abd.2021.09.008 |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
text/html |
dc.publisher.none.fl_str_mv |
Sociedade Brasileira de Dermatologia |
publisher.none.fl_str_mv |
Sociedade Brasileira de Dermatologia |
dc.source.none.fl_str_mv |
Anais Brasileiros de Dermatologia v.97 n.4 2022 reponame:Anais brasileiros de dermatologia (Online) instname:Sociedade Brasileira de Dermatologia (SBD) instacron:SBD |
instname_str |
Sociedade Brasileira de Dermatologia (SBD) |
instacron_str |
SBD |
institution |
SBD |
reponame_str |
Anais brasileiros de dermatologia (Online) |
collection |
Anais brasileiros de dermatologia (Online) |
repository.name.fl_str_mv |
Anais brasileiros de dermatologia (Online) - Sociedade Brasileira de Dermatologia (SBD) |
repository.mail.fl_str_mv |
abd@sbd.org.br||revista@sbd.org.br |
_version_ |
1752126424933728256 |