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dc.contributor.authorYu, Xinhuazh_CN
dc.contributor.authorZheng, Junfengzh_CN
dc.contributor.authorCollin, Mattiaszh_CN
dc.contributor.authorSchmidt, Ennozh_CN
dc.contributor.authorZillikens, Detlefzh_CN
dc.contributor.authorPetersen, Frankzh_CN
dc.contributor.author余新华zh_CN
dc.date.accessioned2015-07-22T07:37:24Z
dc.date.available2015-07-22T07:37:24Z
dc.date.issued2014-02-04zh_CN
dc.identifier.citationPLOS ONE, 2014,9(2):-zh_CN
dc.identifier.otherWOS:000330631800005zh_CN
dc.identifier.urihttps://dspace.xmu.edu.cn/handle/2288/93669
dc.descriptionDeutsche Forschungsgemeinschaft, Cluster of Excellence "Inflammation at Interfaces" [EXC 306/1, EXC 306/2]; Swedish Research Council [2010-57X-20240]; Foundation of Ake Wiberg; Foundation of Alfred Osterlund; Foundation of King Gustaf V's 80 years fund; Foundation of Hansa Medical AB; Medical College of Xiamen Universityzh_CN
dc.description.abstractEndo-beta-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 gamma 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.zh_CN
dc.language.isoen_USzh_CN
dc.publisherPUBLIC LIBRARY SCIENCEzh_CN
dc.source.urihttp://dx.doi.org/10.1371/journal.pone.0085317zh_CN
dc.subjectDERMAL-EPIDERMAL SEPARATIONzh_CN
dc.subjectINDUCED TISSUE-DAMAGEzh_CN
dc.subjectGLYCAN HYDROLYSISzh_CN
dc.subjectVII COLLAGENzh_CN
dc.subjectSTREPTOCOCCUS-PYOGENESzh_CN
dc.subjectGLYCOSYLATIONzh_CN
dc.subjectAUTOANTIBODIESzh_CN
dc.subjectACTIVATIONzh_CN
dc.subjectINDUCTIONzh_CN
dc.subjectIMPACTzh_CN
dc.titleEndoS Reduces the Pathogenicity of Anti-mCOL7 IgG through Reduced Binding of Immune Complexes to Neutrophilszh_CN
dc.typeArticlezh_CN


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