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http://purl.uniprot.org/citations/24453251http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/24453251http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/24453251http://www.w3.org/2000/01/rdf-schema#comment"Inhibition of B cells constitutes a rational approach for treating B cell-mediated disorders. We demonstrate in this article that the engagement of the surface Ig-like transcript 2 (ILT2) inhibitory receptor with its preferential ligand HLA-G is critical to inhibit B cell functions. Indeed, ILT2-HLA-G interaction impedes both naive and memory B cell functions in vitro and in vivo. Particularly, HLA-G inhibits B cell proliferation, differentiation, and Ig secretion in both T cell-dependent and -independent models of B cell activation. HLA-G mediates phenotypic and functional downregulation of CXCR4 and CXCR5 chemokine receptors on germinal center B cells. In-depth analysis of the molecular mechanisms mediated by ILT2-HLA-G interaction showed a G0/G1 cell cycle arrest through dephosphorylation of AKT, GSK-3β, c-Raf, and Foxo proteins. Crucially, we provide in vivo evidence that HLA-G acts as a negative B cell regulator in modulating B cell Ab secretion in a xenograft mouse model. This B cell regulatory mechanism involving ILT2-HLA-G interaction brings important insight to design future B cell-targeted therapies aimed at reducing inappropriate immune reaction in allotransplantation and autoimmune diseases."xsd:string
http://purl.uniprot.org/citations/24453251http://purl.org/dc/terms/identifier"doi:10.4049/jimmunol.1300438"xsd:string
http://purl.uniprot.org/citations/24453251http://purl.org/dc/terms/identifier"doi:10.4049/jimmunol.1300438"xsd:string
http://purl.uniprot.org/citations/24453251http://purl.uniprot.org/core/author"Morandi F."xsd:string
http://purl.uniprot.org/citations/24453251http://purl.uniprot.org/core/author"Morandi F."xsd:string
http://purl.uniprot.org/citations/24453251http://purl.uniprot.org/core/author"Naji A."xsd:string
http://purl.uniprot.org/citations/24453251http://purl.uniprot.org/core/author"Naji A."xsd:string
http://purl.uniprot.org/citations/24453251http://purl.uniprot.org/core/author"Ferretti E."xsd:string
http://purl.uniprot.org/citations/24453251http://purl.uniprot.org/core/author"Ferretti E."xsd:string
http://purl.uniprot.org/citations/24453251http://purl.uniprot.org/core/author"Agaugue S."xsd:string
http://purl.uniprot.org/citations/24453251http://purl.uniprot.org/core/author"Agaugue S."xsd:string
http://purl.uniprot.org/citations/24453251http://purl.uniprot.org/core/author"Bruel S."xsd:string
http://purl.uniprot.org/citations/24453251http://purl.uniprot.org/core/author"Bruel S."xsd:string
http://purl.uniprot.org/citations/24453251http://purl.uniprot.org/core/author"Carosella E.D."xsd:string
http://purl.uniprot.org/citations/24453251http://purl.uniprot.org/core/author"Carosella E.D."xsd:string
http://purl.uniprot.org/citations/24453251http://purl.uniprot.org/core/author"Maki G."xsd:string
http://purl.uniprot.org/citations/24453251http://purl.uniprot.org/core/author"Maki G."xsd:string
http://purl.uniprot.org/citations/24453251http://purl.uniprot.org/core/author"Menier C."xsd:string
http://purl.uniprot.org/citations/24453251http://purl.uniprot.org/core/author"Menier C."xsd:string
http://purl.uniprot.org/citations/24453251http://purl.uniprot.org/core/author"Pistoia V."xsd:string
http://purl.uniprot.org/citations/24453251http://purl.uniprot.org/core/author"Pistoia V."xsd:string
http://purl.uniprot.org/citations/24453251http://purl.uniprot.org/core/author"Rouas-Freiss N."xsd:string
http://purl.uniprot.org/citations/24453251http://purl.uniprot.org/core/author"Rouas-Freiss N."xsd:string