| http://purl.uniprot.org/citations/24523933 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/24523933 | http://www.w3.org/2000/01/rdf-schema#comment | "Anti-glycan/ganglioside antibodies are the most common immune effectors found in patients with Guillain-Barré Syndrome, which is a peripheral autoimmune neuropathy. We previously reported that disease-relevant anti-glycan autoantibodies inhibited axon regeneration, which echo the clinical association of these antibodies and poor recovery in Guillain-Barré Syndrome. However, the specific molecular and cellular elements involved in this antibody-mediated inhibition of axon regeneration are not previously defined. This study examined the role of Fcγ receptors and macrophages in the antibody-mediated inhibition of axon regeneration. A well characterized antibody passive transfer sciatic nerve crush and transplant models were used to study the anti-ganglioside antibody-mediated inhibition of axon regeneration in wild type and various mutant and transgenic mice with altered expression of specific Fcγ receptors and macrophage/microglia populations. Outcome measures included behavior, electrophysiology, morphometry, immunocytochemistry, quantitative real-time PCR, and western blotting. We demonstrate that the presence of autoantibodies, directed against neuronal/axonal cell surface gangliosides, in the injured mammalian peripheral nerves switch the proregenerative inflammatory environment to growth inhibitory milieu by engaging specific activating Fcγ receptors on recruited monocyte-derived macrophages to cause severe inhibition of axon regeneration. Our data demonstrate that the antibody orchestrated Fcγ receptor-mediated switch in inflammation is one mechanism underlying inhibition of axon regeneration. These findings have clinical implications for nerve repair and recovery in antibody-mediated immune neuropathies. Our results add to the complexity of axon regeneration in injured peripheral and central nervous systems as adverse effects of B cells and autoantibodies on neural injury and repair are increasingly recognized."xsd:string |
| http://purl.uniprot.org/citations/24523933 | http://purl.org/dc/terms/identifier | "doi:10.1371/journal.pone.0088703"xsd:string |
| http://purl.uniprot.org/citations/24523933 | http://purl.uniprot.org/core/author | "Zhang G."xsd:string |
| http://purl.uniprot.org/citations/24523933 | http://purl.uniprot.org/core/author | "Gao T."xsd:string |
| http://purl.uniprot.org/citations/24523933 | http://purl.uniprot.org/core/author | "Song J.J."xsd:string |
| http://purl.uniprot.org/citations/24523933 | http://purl.uniprot.org/core/author | "Bogdanova N."xsd:string |
| http://purl.uniprot.org/citations/24523933 | http://purl.uniprot.org/core/author | "Sheikh K.A."xsd:string |
| http://purl.uniprot.org/citations/24523933 | http://purl.uniprot.org/core/author | "Glennie M.J."xsd:string |
| http://purl.uniprot.org/citations/24523933 | http://purl.uniprot.org/core/author | "Cragg M.S."xsd:string |
| http://purl.uniprot.org/citations/24523933 | http://purl.uniprot.org/core/date | "2014"xsd:gYear |
| http://purl.uniprot.org/citations/24523933 | http://purl.uniprot.org/core/name | "PLoS One"xsd:string |
| http://purl.uniprot.org/citations/24523933 | http://purl.uniprot.org/core/pages | "e88703"xsd:string |
| http://purl.uniprot.org/citations/24523933 | http://purl.uniprot.org/core/title | "Fcgamma receptor-mediated inflammation inhibits axon regeneration."xsd:string |
| http://purl.uniprot.org/citations/24523933 | http://purl.uniprot.org/core/volume | "9"xsd:string |
| http://purl.uniprot.org/citations/24523933 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/24523933 |
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