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EndoS reduces the pathogenicity of anti-mCOL7 IgG through reduced binding of immune complexes to neutrophils.

ABSTRACT: Endo-?-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 Fc?R on neutrophils. On the basis of this newly identified EndoS-mediated mechanism we hope to develop new strategies in the treatment of the disease.

SUBMITTER: Yu X

PROVIDER: S-EPMC3913582 | biostudies-literature | 2014

REPOSITORIES: biostudies-literature

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EndoS reduces the pathogenicity of anti-mCOL7 IgG through reduced binding of immune complexes to neutrophils.

Yu Xinhua X Zheng Junfeng J Collin Mattias M Schmidt Enno E Zillikens Detlef D Petersen Frank F

PloS one 20140204 2

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 b ...[more]

PMID: 24504190

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Blocking FcRn in humans reduces circulating IgG levels and inhibits IgG immune complex-mediated immune responses.

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The Pathogenicity of Anti-?2GP1-IgG Autoantibodies Depends on Fc Glycosylation.

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Evidence that FcRn mediates the transplacental passage of maternal IgE in the form of IgG anti-IgE/IgE immune complexes.

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| S-EPMC4437844 | biostudies-literature

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| S-EPMC7273830 | biostudies-literature

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