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Astrocytic junctional adhesion molecule-A regulates T-cell entry past the glia limitans to promote central nervous system autoimmune attack.

dc.rights.licenseopenen_US
dc.contributor.authorAMATRUDA, Mario
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorCHAPOULY, Candice
dc.contributor.authorWOO, Viola
dc.contributor.authorSAFAVI, Farinaz
dc.contributor.authorZHANG, Joy
dc.contributor.authorDAI, David
dc.contributor.authorTHERATTIL, Anthony
dc.contributor.authorMOON, Chang
dc.contributor.authorVILLAVICENCIO, Jorge
dc.contributor.authorGORDON, Alexandra
dc.contributor.authorPARKOS, Charles
dc.contributor.authorHORNG, Sam
dc.date.accessioned2022-04-07T10:20:02Z
dc.date.available2022-04-07T10:20:02Z
dc.date.issued2022-01-01
dc.identifier.issn2632-1297en_US
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/136606
dc.description.abstractEnContact-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.isoENen_US
dc.subjectARTICLE RECHERCHE
dc.title.enAstrocytic junctional adhesion molecule-A regulates T-cell entry past the glia limitans to promote central nervous system autoimmune attack.
dc.title.alternativeBrain Communen_US
dc.typeArticle de revueen_US
dc.identifier.doi10.1093/braincomms/fcac044en_US
dc.subject.halSciences du Vivant [q-bio]en_US
dc.identifier.pubmed35265839en_US
bordeaux.journalBrain Communicationsen_US
bordeaux.pagefcac044en_US
bordeaux.volume4en_US
bordeaux.hal.laboratoriesBiologie des maladies cardiovasculaires (BMC) - UMR 1034en_US
bordeaux.issue2en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.institutionINSERMen_US
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
bordeaux.import.sourcepubmed
hal.exportfalse
workflow.import.sourcepubmed
dc.rights.ccPas de Licence CCen_US
bordeaux.COinSctx_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


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