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IgA Vasculitis: Etiology, Treatment, Biomarkers and Epigenetic Changes

IgA, previously called Henoch-Schönlein vasculitis, is an essential immune component that drives the host immune response to the external environment. As IgA has the unique characteristic of a flexible response to broad types of microorganisms, it sometimes causes an autoreactive response in the hos...

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Detalles Bibliográficos
Autores principales: Sugino, Hitomi, Sawada, Yu, Nakamura, Motonobu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8307949/
https://www.ncbi.nlm.nih.gov/pubmed/34299162
http://dx.doi.org/10.3390/ijms22147538
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author Sugino, Hitomi
Sawada, Yu
Nakamura, Motonobu
author_facet Sugino, Hitomi
Sawada, Yu
Nakamura, Motonobu
author_sort Sugino, Hitomi
collection PubMed
description IgA, previously called Henoch-Schönlein vasculitis, is an essential immune component that drives the host immune response to the external environment. As IgA has the unique characteristic of a flexible response to broad types of microorganisms, it sometimes causes an autoreactive response in the host human body. IgA vasculitis and related organ dysfunction are representative IgA-mediated autoimmune diseases; bacterial and viral infections often trigger IgA vasculitis. Recent drug developments and the presence of COVID-19 have revealed that these agents can also trigger IgA vasculitis. These findings provide a novel understanding of the pathogenesis of IgA vasculitis. In this review, we focus on the characteristics of IgA and symptoms of IgA vasculitis and other organ dysfunction. We also mention the therapeutic approach, biomarkers, novel triggers for IgA vasculitis, and epigenetic modifications in patients with IgA vasculitis.
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spelling pubmed-83079492021-07-25 IgA Vasculitis: Etiology, Treatment, Biomarkers and Epigenetic Changes Sugino, Hitomi Sawada, Yu Nakamura, Motonobu Int J Mol Sci Review IgA, previously called Henoch-Schönlein vasculitis, is an essential immune component that drives the host immune response to the external environment. As IgA has the unique characteristic of a flexible response to broad types of microorganisms, it sometimes causes an autoreactive response in the host human body. IgA vasculitis and related organ dysfunction are representative IgA-mediated autoimmune diseases; bacterial and viral infections often trigger IgA vasculitis. Recent drug developments and the presence of COVID-19 have revealed that these agents can also trigger IgA vasculitis. These findings provide a novel understanding of the pathogenesis of IgA vasculitis. In this review, we focus on the characteristics of IgA and symptoms of IgA vasculitis and other organ dysfunction. We also mention the therapeutic approach, biomarkers, novel triggers for IgA vasculitis, and epigenetic modifications in patients with IgA vasculitis. MDPI 2021-07-14 /pmc/articles/PMC8307949/ /pubmed/34299162 http://dx.doi.org/10.3390/ijms22147538 Text en © 2021 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Sugino, Hitomi
Sawada, Yu
Nakamura, Motonobu
IgA Vasculitis: Etiology, Treatment, Biomarkers and Epigenetic Changes
title IgA Vasculitis: Etiology, Treatment, Biomarkers and Epigenetic Changes
title_full IgA Vasculitis: Etiology, Treatment, Biomarkers and Epigenetic Changes
title_fullStr IgA Vasculitis: Etiology, Treatment, Biomarkers and Epigenetic Changes
title_full_unstemmed IgA Vasculitis: Etiology, Treatment, Biomarkers and Epigenetic Changes
title_short IgA Vasculitis: Etiology, Treatment, Biomarkers and Epigenetic Changes
title_sort iga vasculitis: etiology, treatment, biomarkers and epigenetic changes
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8307949/
https://www.ncbi.nlm.nih.gov/pubmed/34299162
http://dx.doi.org/10.3390/ijms22147538
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