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

Yu, Xinhua; Zheng, Junfeng; Collin, Mattias LU ; Schmidt, Enno; Zillikens, Detlef and Petersen, Frank (2014) In PLoS ONE 9(2).
Abstract
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.
Please use this url to cite or link to this publication:
author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
PLoS ONE
volume
9
issue
2
publisher
Public Library of Science
external identifiers
  • pmid:24504190
  • wos:000330631800005
  • scopus:84896866511
ISSN
1932-6203
DOI
10.1371/journal.pone.0085317
language
English
LU publication?
yes
id
12556fa1-78fd-42d1-912b-bf3339e22118 (old id 4335435)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/24504190?dopt=Abstract
date added to LUP
2014-03-06 19:43:49
date last changed
2017-01-01 05:42:12
@article{12556fa1-78fd-42d1-912b-bf3339e22118,
  abstract     = {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.},
  articleno    = {e85317},
  author       = {Yu, Xinhua and Zheng, Junfeng and Collin, Mattias and Schmidt, Enno and Zillikens, Detlef and Petersen, Frank},
  issn         = {1932-6203},
  language     = {eng},
  number       = {2},
  publisher    = {Public Library of Science},
  series       = {PLoS ONE},
  title        = {EndoS Reduces the Pathogenicity of Anti-mCOL7 IgG through Reduced Binding of Immune Complexes to Neutrophils.},
  url          = {http://dx.doi.org/10.1371/journal.pone.0085317},
  volume       = {9},
  year         = {2014},
}