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Vitiligo: An Autoimmune Skin Disease and its Immunomodulatory Therapeutic Intervention

Vitiligo is a chronic autoimmune depigmenting skin disorder characterized by patches of the skin losing functional melanocytes. Multiple combinatorial factors are involved in disease development, among which immune T cells play a prominent role. The immune cells implicated in melanocyte destruction...

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Autores principales: Chang, Wei-Ling, Lee, Woan-Ruoh, Kuo, Yung-Che, Huang, Yen-Hua
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8712646/
https://www.ncbi.nlm.nih.gov/pubmed/34970551
http://dx.doi.org/10.3389/fcell.2021.797026
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author Chang, Wei-Ling
Lee, Woan-Ruoh
Kuo, Yung-Che
Huang, Yen-Hua
author_facet Chang, Wei-Ling
Lee, Woan-Ruoh
Kuo, Yung-Che
Huang, Yen-Hua
author_sort Chang, Wei-Ling
collection PubMed
description Vitiligo is a chronic autoimmune depigmenting skin disorder characterized by patches of the skin losing functional melanocytes. Multiple combinatorial factors are involved in disease development, among which immune T cells play a prominent role. The immune cells implicated in melanocyte destruction through adaptive immunity include CD8(+) cytotoxic T cells and regulatory T cells, and aberrantly activated skin-resident memory T cells also play a role in melanocyte destruction. Over the past several years, major progress in understanding vitiligo pathogenesis has led to the development of targeted therapies. Janus kinase (JAK) inhibitors, which share the similar mechanism that autoactivates CD8(+) T cells in chronic inflammatory diseases, have been reported to have therapeutic significance in vitiligo. Recently, immunomodulatory therapeutic interventions in vitiligo have been emerging. Mesenchymal stem cells (MSCs) regulate cytokine secretion and the balance of T-cell subsets, which makes them a promising cell-based treatment option for autoimmune diseases. The induction of MSC-mediated immunomodulation is complicated and occurs by contact-dependent mechanisms and soluble extracellular vesicle (EV) mediators. EVs released from MSCs contain various growth factors and cytokines with anti-inflammatory effects in the skin immune response. Here, we summarize and discuss the progress to date in targeted therapies that immunomodulate the niche environment of vitiligo, from the clinical trial of JAK inhibitors to the potential of MSCs and MSC-EVs. The available information was collected to highlight the need for further research into the treatment of vitiligo.
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spelling pubmed-87126462021-12-29 Vitiligo: An Autoimmune Skin Disease and its Immunomodulatory Therapeutic Intervention Chang, Wei-Ling Lee, Woan-Ruoh Kuo, Yung-Che Huang, Yen-Hua Front Cell Dev Biol Cell and Developmental Biology Vitiligo is a chronic autoimmune depigmenting skin disorder characterized by patches of the skin losing functional melanocytes. Multiple combinatorial factors are involved in disease development, among which immune T cells play a prominent role. The immune cells implicated in melanocyte destruction through adaptive immunity include CD8(+) cytotoxic T cells and regulatory T cells, and aberrantly activated skin-resident memory T cells also play a role in melanocyte destruction. Over the past several years, major progress in understanding vitiligo pathogenesis has led to the development of targeted therapies. Janus kinase (JAK) inhibitors, which share the similar mechanism that autoactivates CD8(+) T cells in chronic inflammatory diseases, have been reported to have therapeutic significance in vitiligo. Recently, immunomodulatory therapeutic interventions in vitiligo have been emerging. Mesenchymal stem cells (MSCs) regulate cytokine secretion and the balance of T-cell subsets, which makes them a promising cell-based treatment option for autoimmune diseases. The induction of MSC-mediated immunomodulation is complicated and occurs by contact-dependent mechanisms and soluble extracellular vesicle (EV) mediators. EVs released from MSCs contain various growth factors and cytokines with anti-inflammatory effects in the skin immune response. Here, we summarize and discuss the progress to date in targeted therapies that immunomodulate the niche environment of vitiligo, from the clinical trial of JAK inhibitors to the potential of MSCs and MSC-EVs. The available information was collected to highlight the need for further research into the treatment of vitiligo. Frontiers Media S.A. 2021-12-14 /pmc/articles/PMC8712646/ /pubmed/34970551 http://dx.doi.org/10.3389/fcell.2021.797026 Text en Copyright © 2021 Chang, Lee, Kuo and Huang. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Cell and Developmental Biology
Chang, Wei-Ling
Lee, Woan-Ruoh
Kuo, Yung-Che
Huang, Yen-Hua
Vitiligo: An Autoimmune Skin Disease and its Immunomodulatory Therapeutic Intervention
title Vitiligo: An Autoimmune Skin Disease and its Immunomodulatory Therapeutic Intervention
title_full Vitiligo: An Autoimmune Skin Disease and its Immunomodulatory Therapeutic Intervention
title_fullStr Vitiligo: An Autoimmune Skin Disease and its Immunomodulatory Therapeutic Intervention
title_full_unstemmed Vitiligo: An Autoimmune Skin Disease and its Immunomodulatory Therapeutic Intervention
title_short Vitiligo: An Autoimmune Skin Disease and its Immunomodulatory Therapeutic Intervention
title_sort vitiligo: an autoimmune skin disease and its immunomodulatory therapeutic intervention
topic Cell and Developmental Biology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8712646/
https://www.ncbi.nlm.nih.gov/pubmed/34970551
http://dx.doi.org/10.3389/fcell.2021.797026
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