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作 者:Morgane Thomas Charlotte Bruzeau Ophélie Alyssa Martin Justine Pollet Sébastien Bender Claire Carrion Sandrine Le Noir Eric Pinaud
机构地区:[1]Laboratoire Contrôle de la Réponse Immune B et des Lymphoproliférations(CRIBL),Universitéde Limoges,CNRS UnitéMixte de Recherche 7276,Inserm Unité1262,Limoges,France [2]Centre Hospitalier Universitaire Dupuytren,Service d’Immunopathologie,Limoges,France [3]Centre Hospitalier Universitaire de Limoges,Centre National de l’Amylose AL et Autres Maladies par Dépôt d’Immunoglobulines Monoclonales,Limoges,France [4]Laboratoire Suivi des Therapies Innovantes,Institut de Genetique Humaine,UMR 9002 CNRS-UM,Montpellier,France
出 处:《Cellular & Molecular Immunology》2023年第10期1114-1126,共13页中国免疫学杂志(英文版)
摘 要:SATB1(Special A-T rich Binding protein 1)is a cell type-specific factor that regulates the genetic network in developing T cells and neurons.In T cells,SATB1 is required for lineage commitment,VDJ recombination,development and maturation.Considering that its expression varies during B-cell differentiation,the involvement of SATB1 needs to be clarified in this lineage.Using a KO mouse model in which SATB1 was deleted from the pro-B-cell stage,we examined the consequences of SATB1 deletion in naive and activated B-cell subsets.Our model indicates first,unlike its essential function in T cells,that SATB1 is dispensable for B-cell development and the establishment of a broad IgH repertoire.Second,we show that SATB1 exhibits an ambivalent function in mature B cells,acting sequentially as a positive and negative regulator of Ig gene transcription in naive and activated cells,respectively.Third,our study indicates that the negative regulatory function of SATB1 in B cells extends to the germinal center response,in which this factor limits somatic hypermutation of Ig genes.
关 键 词:B cells Nuclear factor Ambivalent Somatic hypermutation
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