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Cytoskeletal Regulation of Inflammation and Its Impact on Skin Blistering Disease Epidermolysis Bullosa Acquisita

Actin remodelling proteins regulate cytoskeletal cell responses and are important in both innate and adaptive immunity. These responses play a major role in providing a fine balance in a cascade of biological events that results in either protective acute inflammation or chronic inflammation that le...

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Detalles Bibliográficos
Autores principales: Kopecki, Zlatko, Ludwig, Ralf J., Cowin, Allison J.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4964491/
https://www.ncbi.nlm.nih.gov/pubmed/27420054
http://dx.doi.org/10.3390/ijms17071116
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author Kopecki, Zlatko
Ludwig, Ralf J.
Cowin, Allison J.
author_facet Kopecki, Zlatko
Ludwig, Ralf J.
Cowin, Allison J.
author_sort Kopecki, Zlatko
collection PubMed
description Actin remodelling proteins regulate cytoskeletal cell responses and are important in both innate and adaptive immunity. These responses play a major role in providing a fine balance in a cascade of biological events that results in either protective acute inflammation or chronic inflammation that leads to a host of diseases including autoimmune inflammation mediated epidermolysis bullosa acquisita (EBA). This review describes the role of the actin cytoskeleton and in particular the actin remodelling protein called Flightless I (Flii) in regulating cellular inflammatory responses and its subsequent effect on the autoimmune skin blistering disease EBA. It also outlines the potential of an antibody based therapy for decreasing Flii expression in vivo to ameliorate the symptoms associated with EBA.
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spelling pubmed-49644912016-08-03 Cytoskeletal Regulation of Inflammation and Its Impact on Skin Blistering Disease Epidermolysis Bullosa Acquisita Kopecki, Zlatko Ludwig, Ralf J. Cowin, Allison J. Int J Mol Sci Review Actin remodelling proteins regulate cytoskeletal cell responses and are important in both innate and adaptive immunity. These responses play a major role in providing a fine balance in a cascade of biological events that results in either protective acute inflammation or chronic inflammation that leads to a host of diseases including autoimmune inflammation mediated epidermolysis bullosa acquisita (EBA). This review describes the role of the actin cytoskeleton and in particular the actin remodelling protein called Flightless I (Flii) in regulating cellular inflammatory responses and its subsequent effect on the autoimmune skin blistering disease EBA. It also outlines the potential of an antibody based therapy for decreasing Flii expression in vivo to ameliorate the symptoms associated with EBA. MDPI 2016-07-13 /pmc/articles/PMC4964491/ /pubmed/27420054 http://dx.doi.org/10.3390/ijms17071116 Text en © 2016 by the authors; 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 (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Kopecki, Zlatko
Ludwig, Ralf J.
Cowin, Allison J.
Cytoskeletal Regulation of Inflammation and Its Impact on Skin Blistering Disease Epidermolysis Bullosa Acquisita
title Cytoskeletal Regulation of Inflammation and Its Impact on Skin Blistering Disease Epidermolysis Bullosa Acquisita
title_full Cytoskeletal Regulation of Inflammation and Its Impact on Skin Blistering Disease Epidermolysis Bullosa Acquisita
title_fullStr Cytoskeletal Regulation of Inflammation and Its Impact on Skin Blistering Disease Epidermolysis Bullosa Acquisita
title_full_unstemmed Cytoskeletal Regulation of Inflammation and Its Impact on Skin Blistering Disease Epidermolysis Bullosa Acquisita
title_short Cytoskeletal Regulation of Inflammation and Its Impact on Skin Blistering Disease Epidermolysis Bullosa Acquisita
title_sort cytoskeletal regulation of inflammation and its impact on skin blistering disease epidermolysis bullosa acquisita
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4964491/
https://www.ncbi.nlm.nih.gov/pubmed/27420054
http://dx.doi.org/10.3390/ijms17071116
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