EndoS Reduces the Pathogenicity of Anti-mCOL7 IgG through Reduced Binding of Immune Complexes to Neutrophils

Endo-β-N-acetylglucosaminidase (EndoS) has been shown to act as a potent pathogen-derived immunomodulatory molecule in autoimmune diseases. Here we investigated how EndoS treatment reduces the pathogenicity of rabbit anti-mCOL7 IgG using different experimental models of epidermolysis bullosa acquisi...

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Autores principales: Yu, Xinhua, Zheng, Junfeng, Collin, Mattias, Schmidt, Enno, Zillikens, Detlef, Petersen, Frank
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2014
Materias:
Research Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3913582/
https://www.ncbi.nlm.nih.gov/pubmed/24504190
http://dx.doi.org/10.1371/journal.pone.0085317
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author Yu, Xinhua
Zheng, Junfeng
Collin, Mattias
Schmidt, Enno
Zillikens, Detlef
Petersen, Frank
author_facet Yu, Xinhua
Zheng, Junfeng
Collin, Mattias
Schmidt, Enno
Zillikens, Detlef
Petersen, Frank
author_sort Yu, Xinhua
collection PubMed
description Endo-β-N-acetylglucosaminidase (EndoS) has been shown to act as a potent pathogen-derived immunomodulatory molecule in autoimmune diseases. Here we investigated how EndoS treatment reduces the pathogenicity of rabbit anti-mCOL7 IgG using different experimental models of epidermolysis bullosa acquisita (EBA). Our results show that the EndoS treatment does not interfere with the binding of the antibody to the antigen but reduces immune complex (IC)-mediated neutrophil activation by impairing the binding of the IC to FcγR on neutrophils. On the basis of this newly identified EndoS-mediated mechanism we hope to develop new strategies in the treatment of the disease.
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spelling pubmed-39135822014-02-06 EndoS Reduces the Pathogenicity of Anti-mCOL7 IgG through Reduced Binding of Immune Complexes to Neutrophils Yu, Xinhua Zheng, Junfeng Collin, Mattias Schmidt, Enno Zillikens, Detlef Petersen, Frank PLoS One Research Article Endo-β-N-acetylglucosaminidase (EndoS) has been shown to act as a potent pathogen-derived immunomodulatory molecule in autoimmune diseases. Here we investigated how EndoS treatment reduces the pathogenicity of rabbit anti-mCOL7 IgG using different experimental models of epidermolysis bullosa acquisita (EBA). Our results show that the EndoS treatment does not interfere with the binding of the antibody to the antigen but reduces immune complex (IC)-mediated neutrophil activation by impairing the binding of the IC to FcγR on neutrophils. On the basis of this newly identified EndoS-mediated mechanism we hope to develop new strategies in the treatment of the disease. Public Library of Science 2014-02-04 /pmc/articles/PMC3913582/ /pubmed/24504190 http://dx.doi.org/10.1371/journal.pone.0085317 Text en © 2014 Yu et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
spellingShingle Research Article
Yu, Xinhua
Zheng, Junfeng
Collin, Mattias
Schmidt, Enno
Zillikens, Detlef
Petersen, Frank
EndoS Reduces the Pathogenicity of Anti-mCOL7 IgG through Reduced Binding of Immune Complexes to Neutrophils
title EndoS Reduces the Pathogenicity of Anti-mCOL7 IgG through Reduced Binding of Immune Complexes to Neutrophils
title_full EndoS Reduces the Pathogenicity of Anti-mCOL7 IgG through Reduced Binding of Immune Complexes to Neutrophils
title_fullStr EndoS Reduces the Pathogenicity of Anti-mCOL7 IgG through Reduced Binding of Immune Complexes to Neutrophils
title_full_unstemmed EndoS Reduces the Pathogenicity of Anti-mCOL7 IgG through Reduced Binding of Immune Complexes to Neutrophils
title_short EndoS Reduces the Pathogenicity of Anti-mCOL7 IgG through Reduced Binding of Immune Complexes to Neutrophils
title_sort endos reduces the pathogenicity of anti-mcol7 igg through reduced binding of immune complexes to neutrophils
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3913582/
https://www.ncbi.nlm.nih.gov/pubmed/24504190
http://dx.doi.org/10.1371/journal.pone.0085317
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