ArticleJournal of neuroinflammation2012
IgG glycan hydrolysis by EndoS inhibits experimental autoimmune encephalomyelitis.
Article in Journal of neuroinflammation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
22 citing papers in PubMed, 35 citations in OpenAlex.
- Immunopathological mechanisms in autoimmune encephalitis: from pathogenesis to targeted therapies.Frontiers in immunology · 2026Review
- Immunomodulating Enzymes fromMicroorganisms · 2024Review
- Reduced serum IgG galactosylation is associated with increased inflammation during relapses of neuromyelitis optica spectrum disorders.Frontiers in immunology · 2024Article
- A subset of type-II collagen-binding antibodies prevents experimental arthritis by inhibiting FCGR3 signaling in neutrophils.Nature communications · 2023Article
- Proteomics, Glycomics, and Glycoproteomics of Matrisome Molecules.Molecular & cellular proteomics : MCP · 2019Review
- Article
- Targeting IgG in Arthritis: Disease Pathways and Therapeutic Avenues.International journal of molecular sciences · 2018Review
- Article
- Characterization of novel endo-β-N-acetylglucosaminidases from Sphingobacterium species, Beauveria bassiana and Cordyceps militaris that specifically hydrolyze fucose-containing oligosaccharides and human IgG.Scientific reports · 2018Article
- Streptococcal Endo-β-Frontiers in immunology · 2018Article
- Regulation of antibody effector functions through IgG Fc N-glycosylation.Cellular and molecular life sciences : CMLS · 2017Review
- CP40 from Corynebacterium pseudotuberculosis is an endo-β-N-acetylglucosaminidase.BMC microbiology · 2016Article
- A novel high mobility group box 1 neutralizing chimeric antibody attenuates drug-induced liver injury and postinjury inflammation in mice.Hepatology (Baltimore, Md.) · 2016Article
- B cell-derived transforming growth factor-β1 expression limits the induction phase of autoimmune neuroinflammation.Scientific reports · 2016Article
- Immune recruitment or suppression by glycan engineering of endogenous and therapeutic antibodies.Biochimica et biophysica acta · 2016Review
- Pro-inflammatory pattern of IgG1 Fc glycosylation in multiple sclerosis cerebrospinal fluid.Journal of neuroinflammation · 2015Article
- Monocyte recruitment by HLA IgG-activated endothelium: the relationship between IgG subclass and FcγRIIa polymorphisms.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2015Article
- B cells in MS and NMO: pathogenesis and therapy.Seminars in immunopathology · 2014Review
- EndoS2 is a unique and conserved enzyme of serotype M49 group A Streptococcus that hydrolyses N-linked glycans on IgG and α1-acid glycoprotein.The Biochemical journal · 2013Article
- Therapeutic potential of deglycosylated antibodies.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Studies in experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis, have shown that B cells markedly influence the course of the disease, although whether their effects are protective or pathological is a matter of debate. EndoS hydrolysis of the IgG glycan has profound effects on IgG effector functions, such as complement activation and Fc receptor binding, suggesting that the enzyme could be used as an immunomodulatory therapeutic agent against IgG-mediated diseases. We demonstrate here that EndoS has a protective effect in myelin oligodendrocyte glycoprotein peptide amino acid 35-55 (MOG(35-55))-induced EAE, a chronic neuroinflammatory demyelinating disorder of the central nervous system (CNS) in which humoral immune responses are thought to play only a minor role. EndoS treatment in chronic MOG(35-55)-EAE did not impair encephalitogenic T cell priming and recruitment into the CNS of mice, consistent with a primary role of EndoS in controlling IgG effector functions. In contrast, reduced EAE severity coincided with poor serum complement activation and deposition within the spinal cord, suggesting that EndoS treatment impairs B cell effector function. These results identify EndoS as a potential therapeutic agent against antibody-mediated CNS autoimmune disorders.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.