RDF/XMLNTriplesTurtleShow queryShare
SubjectPredicateObject
http://purl.uniprot.org/citations/29643191http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/29643191http://www.w3.org/2000/01/rdf-schema#comment"Anti-CD83 Ab capable of Ab-dependent cellular cytotoxicity can deplete activated CD83+ human dendritic cells, thereby inhibiting CD4 T cell-mediated acute graft-versus-host disease. As CD83 is also expressed on the surface of activated B lymphocytes, we hypothesized that anti-CD83 would also inhibit B cell responses to stimulation. We found that anti-CD83 inhibited total IgM and IgG production in vitro by allostimulated human PBMC. Also, Ag-specific Ab responses to immunization of SCID mice xenografted with human PBMC were inhibited by anti-CD83 treatment. This inhibition occurred without depletion of all human B cells because anti-CD83 lysed activated CD83+ B cells by Ab-dependent cellular cytotoxicity and spared resting (CD83-) B cells. In cultured human PBMC, anti-CD83 inhibited tetanus toxoid-stimulated B cell proliferation and concomitant dendritic cell-mediated CD4 T cell proliferation and expression of IFN-γ and IL-17A, with minimal losses of B cells (<20%). In contrast, the anti-CD20 mAb rituximab depleted >80% of B cells but had no effect on CD4 T cell proliferation and cytokine expression. By virtue of the ability of anti-CD83 to selectively deplete activated, but not resting, B cells and dendritic cells, with the latter reducing CD4 T cell responses, anti-CD83 may be clinically useful in autoimmunity and transplantation. Advantages might include inhibited expansion of autoantigen- or alloantigen-specific B cells and CD4 T cells, thus preventing further production of pathogenic Abs and inflammatory cytokines while preserving protective memory and regulatory cells."xsd:string
http://purl.uniprot.org/citations/29643191http://purl.org/dc/terms/identifier"doi:10.4049/jimmunol.1700064"xsd:string
http://purl.uniprot.org/citations/29643191http://purl.uniprot.org/core/author"Jones M.L."xsd:string
http://purl.uniprot.org/citations/29643191http://purl.uniprot.org/core/author"Baron R."xsd:string
http://purl.uniprot.org/citations/29643191http://purl.uniprot.org/core/author"Munster D.J."xsd:string
http://purl.uniprot.org/citations/29643191http://purl.uniprot.org/core/author"Wong K.Y."xsd:string
http://purl.uniprot.org/citations/29643191http://purl.uniprot.org/core/author"Rice A.M."xsd:string
http://purl.uniprot.org/citations/29643191http://purl.uniprot.org/core/author"Seldon T.A."xsd:string
http://purl.uniprot.org/citations/29643191http://purl.uniprot.org/core/date"2018"xsd:gYear
http://purl.uniprot.org/citations/29643191http://purl.uniprot.org/core/name"J Immunol"xsd:string
http://purl.uniprot.org/citations/29643191http://purl.uniprot.org/core/pages"3383-3396"xsd:string
http://purl.uniprot.org/citations/29643191http://purl.uniprot.org/core/title"CD83 Antibody Inhibits Human B Cell Responses to Antigen as well as Dendritic Cell-Mediated CD4 T Cell Responses."xsd:string
http://purl.uniprot.org/citations/29643191http://purl.uniprot.org/core/volume"200"xsd:string
http://purl.uniprot.org/citations/29643191http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/29643191
http://purl.uniprot.org/citations/29643191http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/29643191
http://purl.uniprot.org/uniprot/#_A0A087WX61-mappedCitation-29643191http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/29643191
http://purl.uniprot.org/uniprot/#_Q01151-mappedCitation-29643191http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/29643191
http://purl.uniprot.org/uniprot/A0A087WX61http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/29643191
http://purl.uniprot.org/uniprot/Q01151http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/29643191