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dc.rights.licenseopenen_US
dc.contributor.authorMICHAUD, Eva
dc.contributor.authorWAECKEL, Louis
dc.contributor.authorGAYET, Remi
dc.contributor.authorGOGUYER-DESCHAUMES, Roman
dc.contributor.authorCHANUT, Blandine
dc.contributor.authorJOSPIN, Fabienne
hal.structure.identifierChimie et Biologie des Membranes et des Nanoobjets [CBMN]
dc.contributor.authorBATHANY, Katell
dc.contributor.authorMONNOYE, Magali
dc.contributor.authorGENET, Coraline
dc.contributor.authorPRIER, Amelie
hal.structure.identifierChimie et Biologie des Membranes et des Nanoobjets [CBMN]
dc.contributor.authorTOKARSKI, Caroline
dc.contributor.authorGÉRARD, Philippe
dc.contributor.authorROBLIN, Xavier
dc.contributor.authorROCHEREAU, Nicolas
dc.contributor.authorPAUL, Stephane
dc.date.accessioned2023-04-26T12:29:29Z
dc.date.available2023-04-26T12:29:29Z
dc.date.issued2022-08-08
dc.identifier.issn1757-4676en_US
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/173214
dc.description.abstractEnAbstract Human secretory immunoglobulins (SIg) A1 and SIgA2 guide mucosal responses toward tolerance or inflammation, notably through reverse-transcytosis, the apical-to-basal transport of IgA2 immune complexes via M cells of gut Peyer's patches. As such, the maintenance of a diverse gut microbiota requires broad affinity IgA and glycan?glycan interaction. Here, we asked whether IgA1 and IgA2-microbiota interactions might be involved in dysbiosis induction during inflammatory bowel diseases. Using stool HPLC-purified IgA, we show that reverse-transcytosis is abrogated in ulcerative colitis (UC) while it is extended to IgA1 in Crohn's disease (CD). 16S RNA sequencing of IgA-bound microbiota in CD and UC showed distinct IgA1- and IgA2-associated microbiota; the IgA1+ fraction of CD microbiota was notably enriched in beneficial commensals. These features were associated with increased IgA anti-glycan reactivity in CD and an opposite loss of reactivity in UC. Our results highlight previously unknown pathogenic properties of IgA in IBD that could support dysbiosis.
dc.language.isoENen_US
dc.rightsAttribution 3.0 United States*
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/us/*
dc.subject.enSIgA
dc.subject.enMicrobiota
dc.subject.enGlycosylation
dc.subject.enIBD
dc.subject.enImmunity
dc.title.enAlteration of microbiota antibody-mediated immune selection contributes to dysbiosis in inflammatory bowel diseases
dc.typeArticle de revueen_US
dc.identifier.doi10.15252/emmm.202115386en_US
dc.subject.halChimie/Matériauxen_US
bordeaux.journalEMBO Molecular Medicineen_US
bordeaux.volume14en_US
bordeaux.hal.laboratoriesCBMN : Chimie & de Biologie des Membranes & des Nano-objets - UMR 5248en_US
bordeaux.issue8en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.institutionBordeaux INPen_US
bordeaux.institutionCNRSen_US
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
hal.exportfalse
dc.rights.ccCC BYen_US
bordeaux.COinSctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=EMBO%20Molecular%20Medicine&rft.date=2022-08-08&rft.volume=14&rft.issue=8&rft.eissn=1757-4676&rft.issn=1757-4676&rft.au=MICHAUD,%20Eva&WAECKEL,%20Louis&GAYET,%20Remi&GOGUYER-DESCHAUMES,%20Roman&CHANUT,%20Blandine&rft.genre=article


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