Astrocytic junctional adhesion molecule-A regulates T-cell entry past the glia limitans to promote central nervous system autoimmune attack.
dc.rights.license | open | en_US |
dc.contributor.author | AMATRUDA, Mario | |
hal.structure.identifier | Biologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases | |
dc.contributor.author | CHAPOULY, Candice | |
dc.contributor.author | WOO, Viola | |
dc.contributor.author | SAFAVI, Farinaz | |
dc.contributor.author | ZHANG, Joy | |
dc.contributor.author | DAI, David | |
dc.contributor.author | THERATTIL, Anthony | |
dc.contributor.author | MOON, Chang | |
dc.contributor.author | VILLAVICENCIO, Jorge | |
dc.contributor.author | GORDON, Alexandra | |
dc.contributor.author | PARKOS, Charles | |
dc.contributor.author | HORNG, Sam | |
dc.date.accessioned | 2022-04-07T10:20:02Z | |
dc.date.available | 2022-04-07T10:20:02Z | |
dc.date.issued | 2022-01-01 | |
dc.identifier.issn | 2632-1297 | en_US |
dc.identifier.uri | https://oskar-bordeaux.fr/handle/20.500.12278/136606 | |
dc.description.abstractEn | Contact-mediated interactions between the astrocytic endfeet and infiltrating immune cells within the perivascular space are underexplored, yet represent potential regulatory check-points against CNS autoimmune disease and disability. Reactive astrocytes upregulate junctional adhesion molecule-A, an immunoglobulin-like cell surface receptor that binds to T cells via its ligand, the integrin, lymphocyte function-associated antigen-1. Here, we tested the role of astrocytic junctional adhesion molecule-A in regulating CNS autoinflammatory disease. In cell co-cultures, we found that junctional adhesion molecule-A-mediated signalling between astrocytes and T cells increases levels of matrix metalloproteinase-2, C-C motif chemokine ligand 2 and granulocyte-macrophage colony-stimulating factor, pro-inflammatory factors driving lymphocyte entry and pathogenicity in multiple sclerosis and experimental autoimmune encephalomyelitis, an animal model of CNS autoimmune disease. In experimental autoimmune encephalomyelitis, mice with astrocyte-specific deletion ( ) exhibit decreased levels of matrix metalloproteinase-2, reduced ability of T cells to infiltrate the CNS parenchyma from the perivascular spaces and a milder histopathological and clinical course of disease compared with wild-type controls ( ). Treatment of wild-type mice with intraperitoneal injection of soluble junctional adhesion molecule-A blocking peptide decreases the severity of experimental autoimmune encephalomyelitis, highlighting the potential of contact-mediated astrocyte-immune cell signalling as a novel translational target against neuroinflammatory disease. | |
dc.language.iso | EN | en_US |
dc.subject | ARTICLE RECHERCHE | |
dc.title.en | Astrocytic junctional adhesion molecule-A regulates T-cell entry past the glia limitans to promote central nervous system autoimmune attack. | |
dc.title.alternative | Brain Commun | en_US |
dc.type | Article de revue | en_US |
dc.identifier.doi | 10.1093/braincomms/fcac044 | en_US |
dc.subject.hal | Sciences du Vivant [q-bio] | en_US |
dc.identifier.pubmed | 35265839 | en_US |
bordeaux.journal | Brain Communications | en_US |
bordeaux.page | fcac044 | en_US |
bordeaux.volume | 4 | en_US |
bordeaux.hal.laboratories | Biologie des maladies cardiovasculaires (BMC) - UMR 1034 | en_US |
bordeaux.issue | 2 | en_US |
bordeaux.institution | Université de Bordeaux | en_US |
bordeaux.institution | INSERM | en_US |
bordeaux.peerReviewed | oui | en_US |
bordeaux.inpress | non | en_US |
bordeaux.import.source | pubmed | |
hal.export | false | |
workflow.import.source | pubmed | |
dc.rights.cc | Pas de Licence CC | en_US |
bordeaux.COinS | ctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=Brain%20Communications&rft.date=2022-01-01&rft.volume=4&rft.issue=2&rft.spage=fcac044&rft.epage=fcac044&rft.eissn=2632-1297&rft.issn=2632-1297&rft.au=AMATRUDA,%20Mario&CHAPOULY,%20Candice&WOO,%20Viola&SAFAVI,%20Farinaz&ZHANG,%20Joy&rft.genre=article |