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dc.rights.licenseopenen_US
dc.contributor.authorPOE, J.C.
dc.contributor.authorFANG, J.
dc.contributor.authorZHANG, D.
dc.contributor.authorLEE, M.R.
dc.contributor.authorDICIOCCIO, R.A.
dc.contributor.authorSU, H.
dc.contributor.authorQIN, X.
dc.contributor.authorZHANG, J.Y.
hal.structure.identifierImmunology from Concept and Experiments to Translation = Immunologie Conceptuelle, Expérimentale et Translationnelle [ImmunoConcept]
dc.contributor.authorVISENTIN, Jonathan
dc.contributor.authorBRACKEN, S.J.
dc.contributor.authorHO, V.T.
dc.contributor.authorWANG, K.S.
dc.contributor.authorROSE, J.J.
dc.contributor.authorPAVLETIC, S.Z.
dc.contributor.authorHAKIM, F.T.
dc.contributor.authorJIA, W.
dc.contributor.authorSUTHERS, A.N.
dc.contributor.authorCURRY-CHISOLM, I.M.
dc.contributor.authorHORWITZ, M.E.
dc.contributor.authorRIZZIERI, D.A.
dc.contributor.authorMCMANIGLE, W.C.
dc.contributor.authorCHAO, N.J.
dc.contributor.authorCARDONES, A.R.
dc.contributor.authorXIE, J.
dc.contributor.authorOWZAR, K.
dc.contributor.authorSARANTOPOULOS, S.
dc.date.accessioned2024-09-25T10:05:42Z
dc.date.available2024-09-25T10:05:42Z
dc.date.issued2023
dc.identifier.issn2379-3708en_US
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/201798
dc.description.abstractEnAlloreactivity can drive autoimmune syndromes. After allogeneic hematopoietic stem cell transplantation (allo-HCT), chronic graft-versus-host disease (cGVHD), a B cell–associated autoimmune-like syndrome, commonly occurs. Because donor-derived B cells continually develop under selective pressure from host alloantigens, aberrant B cell receptor (BCR) activation and IgG production can emerge and contribute to cGVHD pathobiology. To better understand molecular programing of B cells in allo-HCT, we performed scRNA-Seq analysis on high numbers of purified B cells from patients. An unsupervised analysis revealed 10 clusters, distinguishable by signature genes for maturation, activation, and memory. Within the memory B cell compartment, we found striking transcriptional differences in allo-HCT patients compared with healthy or infected individuals, including potentially pathogenic atypical B cells (ABCs) that were expanded in active cGVHD. To identify intrinsic alterations in potentially pathological B cells, we interrogated all clusters for differentially expressed genes (DEGs) in active cGVHD versus patients who never had signs of immune tolerance loss (no cGVHD). Active cGVHD DEGs occurred in both naive and BCR-activated B cell clusters. Remarkably, some DEGs occurred across most clusters, suggesting common molecular programs that may promote B cell plasticity. Our study of human allo-HCT and cGVHD provides understanding of altered B cell memory during chronic alloantigen stimulation.
dc.language.isoENen_US
dc.rightsAttribution 3.0 United States*
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/us/*
dc.subject.enAutoimmune diseases
dc.subject.enBone marrow transplantation
dc.subject.enImmunology
dc.subject.enTolerance
dc.title.enSingle-cell landscape analysis unravels molecular programming of the human B cell compartment in chronic GVHD
dc.typeArticle de revueen_US
dc.identifier.doi10.1172/jci.insight.169732en_US
dc.subject.halSciences du Vivant [q-bio]/Immunologieen_US
dc.identifier.pubmed37129971en_US
bordeaux.journalJCI Insighten_US
bordeaux.volume8en_US
bordeaux.hal.laboratoriesImmunoConcEpT - UMR 5164en_US
bordeaux.issue11en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.institutionCNRSen_US
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
hal.identifierhal-04709027
hal.version1
hal.date.transferred2024-09-25T10:05:48Z
hal.popularnonen_US
hal.audienceInternationaleen_US
hal.exporttrue
dc.rights.ccCC BYen_US
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