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Lymphoid Stress Surveillance Response Contributes to Vitiligo Pathogenesis

Vitiligo is a chronic multifactorial depigmentation disorder characterized by the destruction and functional loss of melanocytes. Although a direct cytotoxic T cell attack is thought to be responsible for melanocyte damage, the events leading to the loss of self-tolerance toward melanocytic antigens...

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Autores principales: Raam, Liisi, Kaleviste, Epp, Šunina, Marina, Vaher, Helen, Saare, Mario, Prans, Ele, Pihlap, Maire, Abram, Kristi, Karelson, Maire, Peterson, Pärt, Rebane, Ana, Kisand, Kai, Kingo, Külli
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6255962/
https://www.ncbi.nlm.nih.gov/pubmed/30515176
http://dx.doi.org/10.3389/fimmu.2018.02707
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author Raam, Liisi
Kaleviste, Epp
Šunina, Marina
Vaher, Helen
Saare, Mario
Prans, Ele
Pihlap, Maire
Abram, Kristi
Karelson, Maire
Peterson, Pärt
Rebane, Ana
Kisand, Kai
Kingo, Külli
author_facet Raam, Liisi
Kaleviste, Epp
Šunina, Marina
Vaher, Helen
Saare, Mario
Prans, Ele
Pihlap, Maire
Abram, Kristi
Karelson, Maire
Peterson, Pärt
Rebane, Ana
Kisand, Kai
Kingo, Külli
author_sort Raam, Liisi
collection PubMed
description Vitiligo is a chronic multifactorial depigmentation disorder characterized by the destruction and functional loss of melanocytes. Although a direct cytotoxic T cell attack is thought to be responsible for melanocyte damage, the events leading to the loss of self-tolerance toward melanocytic antigens are not understood. This research aimed to identify novel cellular and molecular factors that participate in vitiligo pathogenesis through the application of gene expression and immunofluorescence analysis of skin biopsy samples along with immunophenotyping of circulating cells. Our study provides insights into the mechanisms involved in melanocyte destruction. The upregulation of stress-ligand MICA/MICB, recognized by activating receptors on innate and innate-like T cells, imply involvement of lymphoid stress surveillance responses in vitiligo lesions. A simultaneous increase in the expression of transcription factor EOMES that is characteristic for innate-like virtual memory T cells, suggest a similar scenario. Local lymphoid stress surveillance has been previously associated with the amplification of systemic humoral responses that were mirrored in our study by increased T follicular helper cells and switched memory B cell proportions in patients with active vitiligo. In addition, microtubule-associated protein light chain 3 staining was compatible with the activation of autophagy in keratinocytes and in the remaining melanocytes of vitiligo lesional skin.
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spelling pubmed-62559622018-12-04 Lymphoid Stress Surveillance Response Contributes to Vitiligo Pathogenesis Raam, Liisi Kaleviste, Epp Šunina, Marina Vaher, Helen Saare, Mario Prans, Ele Pihlap, Maire Abram, Kristi Karelson, Maire Peterson, Pärt Rebane, Ana Kisand, Kai Kingo, Külli Front Immunol Immunology Vitiligo is a chronic multifactorial depigmentation disorder characterized by the destruction and functional loss of melanocytes. Although a direct cytotoxic T cell attack is thought to be responsible for melanocyte damage, the events leading to the loss of self-tolerance toward melanocytic antigens are not understood. This research aimed to identify novel cellular and molecular factors that participate in vitiligo pathogenesis through the application of gene expression and immunofluorescence analysis of skin biopsy samples along with immunophenotyping of circulating cells. Our study provides insights into the mechanisms involved in melanocyte destruction. The upregulation of stress-ligand MICA/MICB, recognized by activating receptors on innate and innate-like T cells, imply involvement of lymphoid stress surveillance responses in vitiligo lesions. A simultaneous increase in the expression of transcription factor EOMES that is characteristic for innate-like virtual memory T cells, suggest a similar scenario. Local lymphoid stress surveillance has been previously associated with the amplification of systemic humoral responses that were mirrored in our study by increased T follicular helper cells and switched memory B cell proportions in patients with active vitiligo. In addition, microtubule-associated protein light chain 3 staining was compatible with the activation of autophagy in keratinocytes and in the remaining melanocytes of vitiligo lesional skin. Frontiers Media S.A. 2018-11-20 /pmc/articles/PMC6255962/ /pubmed/30515176 http://dx.doi.org/10.3389/fimmu.2018.02707 Text en Copyright © 2018 Raam, Kaleviste, Šunina, Vaher, Saare, Prans, Pihlap, Abram, Karelson, Peterson, Rebane, Kisand and Kingo. http://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 Immunology
Raam, Liisi
Kaleviste, Epp
Šunina, Marina
Vaher, Helen
Saare, Mario
Prans, Ele
Pihlap, Maire
Abram, Kristi
Karelson, Maire
Peterson, Pärt
Rebane, Ana
Kisand, Kai
Kingo, Külli
Lymphoid Stress Surveillance Response Contributes to Vitiligo Pathogenesis
title Lymphoid Stress Surveillance Response Contributes to Vitiligo Pathogenesis
title_full Lymphoid Stress Surveillance Response Contributes to Vitiligo Pathogenesis
title_fullStr Lymphoid Stress Surveillance Response Contributes to Vitiligo Pathogenesis
title_full_unstemmed Lymphoid Stress Surveillance Response Contributes to Vitiligo Pathogenesis
title_short Lymphoid Stress Surveillance Response Contributes to Vitiligo Pathogenesis
title_sort lymphoid stress surveillance response contributes to vitiligo pathogenesis
topic Immunology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6255962/
https://www.ncbi.nlm.nih.gov/pubmed/30515176
http://dx.doi.org/10.3389/fimmu.2018.02707
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