http://purl.uniprot.org/citations/34382069 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/34382069 | http://www.w3.org/2000/01/rdf-schema#comment | "ObjectivesChemokines (CKs) are key players of immune-cell homing and differentiation. CK receptors (CKRs) can be used to define T-cell functional subsets. We aimed to characterize the CKR profile of the regulatory B-cell subset B10+ cells and investigate the CKs involved in their migration and differentiation in healthy donors and patients with RA.MethodsRNA sequencing and cytometry were used to compare CKR expression between B10+ and B10neg cells. Migration of B10+ and B10neg cells and IL-10 secretion of B cells in response to recombinant CKs or synovial fluid (SF) were assessed.ResultsCXCR5 was expressed at a higher level on the B10+ cell surface as compared with other B cells (referred to as B10neg cells). In line with this, its ligand CXCL13 preferentially attracted B10+ cells over B10neg cells. Interestingly, synovial fluid from RA patients contained high levels of CXCL13 and induced strong and preferential migration of B10+ cells. Besides its role in attracting B10+ cells, CXCL13 also promoted IL-10 secretion by B cells. In RA patients, the level of CXCR5 on B-cell surface was reduced. The preferential migration of RA B10+ cells toward CXCL13-rich SF was lost and CXCL13 stimulation triggered less IL-10 secretion than in healthy donors.ConclusionOur results identify that the CXCR5/CXCL13 axis is essential for B10+ cell biology but is defective in RA. Restoring the preferential migration of B10+ within the affected joints to better control inflammation may be part of the therapeutic approach for RA."xsd:string |
http://purl.uniprot.org/citations/34382069 | http://purl.org/dc/terms/identifier | "doi:10.1093/rheumatology/keab639"xsd:string |
http://purl.uniprot.org/citations/34382069 | http://purl.uniprot.org/core/author | "Schreiber K."xsd:string |
http://purl.uniprot.org/citations/34382069 | http://purl.uniprot.org/core/author | "Macia L."xsd:string |
http://purl.uniprot.org/citations/34382069 | http://purl.uniprot.org/core/author | "Combe B."xsd:string |
http://purl.uniprot.org/citations/34382069 | http://purl.uniprot.org/core/author | "Morel J."xsd:string |
http://purl.uniprot.org/citations/34382069 | http://purl.uniprot.org/core/author | "Corbeau P."xsd:string |
http://purl.uniprot.org/citations/34382069 | http://purl.uniprot.org/core/author | "Audo R."xsd:string |
http://purl.uniprot.org/citations/34382069 | http://purl.uniprot.org/core/author | "Daien C.I."xsd:string |
http://purl.uniprot.org/citations/34382069 | http://purl.uniprot.org/core/author | "Mielle J."xsd:string |
http://purl.uniprot.org/citations/34382069 | http://purl.uniprot.org/core/author | "Rempenault C."xsd:string |
http://purl.uniprot.org/citations/34382069 | http://purl.uniprot.org/core/date | "2022"xsd:gYear |
http://purl.uniprot.org/citations/34382069 | http://purl.uniprot.org/core/name | "Rheumatology (Oxford)"xsd:string |
http://purl.uniprot.org/citations/34382069 | http://purl.uniprot.org/core/pages | "2185-2196"xsd:string |
http://purl.uniprot.org/citations/34382069 | http://purl.uniprot.org/core/title | "CXCR5/CXCL13 pathway, a key driver for migration of regulatory B10 cells, is defective in patients with rheumatoid arthritis."xsd:string |
http://purl.uniprot.org/citations/34382069 | http://purl.uniprot.org/core/volume | "61"xsd:string |
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