EndoS reduces the pathogenicity of anti-mCOL7 IgG through reduced binding of immune complexes to neutrophils.
basic_science · Level V
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- Record sourced from PubMed, PMID 24504190.
- Also identified by DOI 10.1371/journal.pone.0085317 and PMC identifier 3913582.
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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.
Medical subject headings
- Antigen-Antibody Complex
- Collagen Type VII
- Immunoglobulin G
- Mannosyl-Glycoprotein Endo-beta-N-Acetylglucosaminidase
- Neutrophils