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Cellular Signaling Pathways in Medium and Large Vessel Vasculitis

Autoimmune and autoinflammatory diseases of the medium and large arteries, including the aorta, cause life-threatening complications due to vessel wall destruction but also by wall remodeling, such as the formation of wall-penetrating microvessels and lumen-stenosing neointima. The two most frequent...

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Autores principales: Watanabe, Ryu, Berry, Gerald J., Liang, David H., Goronzy, Jörg J., Weyand, Cornelia M.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7544845/
https://www.ncbi.nlm.nih.gov/pubmed/33072134
http://dx.doi.org/10.3389/fimmu.2020.587089
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author Watanabe, Ryu
Berry, Gerald J.
Liang, David H.
Goronzy, Jörg J.
Weyand, Cornelia M.
author_facet Watanabe, Ryu
Berry, Gerald J.
Liang, David H.
Goronzy, Jörg J.
Weyand, Cornelia M.
author_sort Watanabe, Ryu
collection PubMed
description Autoimmune and autoinflammatory diseases of the medium and large arteries, including the aorta, cause life-threatening complications due to vessel wall destruction but also by wall remodeling, such as the formation of wall-penetrating microvessels and lumen-stenosing neointima. The two most frequent large vessel vasculitides, giant cell arteritis (GCA) and Takayasu arteritis (TAK), are HLA-associated diseases, strongly suggestive for a critical role of T cells and antigen recognition in disease pathogenesis. Recent studies have revealed a growing spectrum of effector functions through which T cells participate in the immunopathology of GCA and TAK; causing the disease-specific patterning of pathology and clinical outcome. Core pathogenic features of disease-relevant T cells rely on the interaction with endothelial cells, dendritic cells and macrophages and lead to vessel wall invasion, formation of tissue-damaging granulomatous infiltrates and induction of the name-giving multinucleated giant cells. Besides antigen, pathogenic T cells encounter danger signals in their immediate microenvironment that they translate into disease-relevant effector functions. Decisive signaling pathways, such as the AKT pathway, the NOTCH pathway, and the JAK/STAT pathway modify antigen-induced T cell activation and emerge as promising therapeutic targets to halt disease progression and, eventually, reset the immune system to reestablish the immune privilege of the arterial wall.
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spelling pubmed-75448452020-10-17 Cellular Signaling Pathways in Medium and Large Vessel Vasculitis Watanabe, Ryu Berry, Gerald J. Liang, David H. Goronzy, Jörg J. Weyand, Cornelia M. Front Immunol Immunology Autoimmune and autoinflammatory diseases of the medium and large arteries, including the aorta, cause life-threatening complications due to vessel wall destruction but also by wall remodeling, such as the formation of wall-penetrating microvessels and lumen-stenosing neointima. The two most frequent large vessel vasculitides, giant cell arteritis (GCA) and Takayasu arteritis (TAK), are HLA-associated diseases, strongly suggestive for a critical role of T cells and antigen recognition in disease pathogenesis. Recent studies have revealed a growing spectrum of effector functions through which T cells participate in the immunopathology of GCA and TAK; causing the disease-specific patterning of pathology and clinical outcome. Core pathogenic features of disease-relevant T cells rely on the interaction with endothelial cells, dendritic cells and macrophages and lead to vessel wall invasion, formation of tissue-damaging granulomatous infiltrates and induction of the name-giving multinucleated giant cells. Besides antigen, pathogenic T cells encounter danger signals in their immediate microenvironment that they translate into disease-relevant effector functions. Decisive signaling pathways, such as the AKT pathway, the NOTCH pathway, and the JAK/STAT pathway modify antigen-induced T cell activation and emerge as promising therapeutic targets to halt disease progression and, eventually, reset the immune system to reestablish the immune privilege of the arterial wall. Frontiers Media S.A. 2020-09-25 /pmc/articles/PMC7544845/ /pubmed/33072134 http://dx.doi.org/10.3389/fimmu.2020.587089 Text en Copyright © 2020 Watanabe, Berry, Liang, Goronzy and Weyand. 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
Watanabe, Ryu
Berry, Gerald J.
Liang, David H.
Goronzy, Jörg J.
Weyand, Cornelia M.
Cellular Signaling Pathways in Medium and Large Vessel Vasculitis
title Cellular Signaling Pathways in Medium and Large Vessel Vasculitis
title_full Cellular Signaling Pathways in Medium and Large Vessel Vasculitis
title_fullStr Cellular Signaling Pathways in Medium and Large Vessel Vasculitis
title_full_unstemmed Cellular Signaling Pathways in Medium and Large Vessel Vasculitis
title_short Cellular Signaling Pathways in Medium and Large Vessel Vasculitis
title_sort cellular signaling pathways in medium and large vessel vasculitis
topic Immunology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7544845/
https://www.ncbi.nlm.nih.gov/pubmed/33072134
http://dx.doi.org/10.3389/fimmu.2020.587089
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