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

Xinhua Yu; Junfeng Zheng; Mattias Collin; Enno Schmidt; Detlef Zillikens; Frank Petersen

doi:10.1371/journal.pone.0085317

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

Xinhua Yu, Junfeng Zheng, Mattias Collin, Enno Schmidt, Detlef Zillikens, Frank Petersen

Klinik für Dermatologie, Allergologie und Venerologie

7 Zitate (Scopus)

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.

Originalsprache	Englisch
Zeitschrift	PLoS ONE
Jahrgang	9
Ausgabenummer	2
ISSN	1553-7390
DOIs	https://doi.org/10.1371/journal.pone.0085317
Publikationsstatus	Veröffentlicht - 04.02.2014

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10.1371/journal.pone.0085317

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title = "EndoS reduces the pathogenicity of anti-mCOL7 IgG through reduced binding of immune complexes to neutrophils",

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.",

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T1 - EndoS reduces the pathogenicity of anti-mCOL7 IgG through reduced binding of immune complexes to neutrophils

AU - Yu, Xinhua

AU - Zheng, Junfeng

AU - Collin, Mattias

AU - Schmidt, Enno

AU - Zillikens, Detlef

AU - Petersen, Frank

PY - 2014/2/4

Y1 - 2014/2/4

N2 - 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.

AB - 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.

U2 - 10.1371/journal.pone.0085317

DO - 10.1371/journal.pone.0085317

M3 - Journal articles

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SN - 1553-7390

VL - 9

JO - PLoS ONE

JF - PLoS ONE

IS - 2

ER -

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

Abstract

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