| http://purl.uniprot.org/citations/22250081 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/22250081 | http://www.w3.org/2000/01/rdf-schema#comment | "The ability of activated B cells to protect against various experimental autoimmune or allergic diseases makes them attractive for use in cell-based therapies. We describe an efficient way to generate B cells with strong suppressive functions by incubating naive B cells with a relevant Ag conjugated to cholera toxin B subunit (CTB). This allows most B cells, irrespective of BCR, to take up and present Ag and induces their expression of latency-associated polypeptide (LAP)/TGF-β and after adoptive transfer also their production of IL-10. With OVA as model Ag, when naive T cells were cocultured in vitro with B cells pretreated with OVA conjugated to CTB (OVA/CTB) Ag-specific CD4(+) Foxp3 regulatory T (Treg) cells increased >50-fold. These cells effectively suppressed CD25(-)CD4(+) effector T (Teff) cells in secondary cultures. Adoptive transfer of OVA/CTB-treated B cells to mice subsequently immunized with OVA in CFA induced increase in Foxp3 Treg cells together with suppression and depletion of Teff cells. Likewise, adoptive transfer of B cells pulsed with myelin oligodendrocyte glycoprotein peptide(35-55) (MOGp) conjugated to CTB increased the number of Treg cells, suppressed MOGp-specific T cell proliferation and IL-17 and IFN-γ production, and prevented the development of experimental autoimmune encephalomyelitis. Similar effects were seen when B cells were given "therapeutically" to mice with early-stage experimental autoimmune encephalomyelitis. Our results suggest that B cells pulsed in vitro with relevant Ag/CTB conjugates may be used in cell therapy to induce Ag-specific suppression of autoimmune disease."xsd:string |
| http://purl.uniprot.org/citations/22250081 | http://purl.org/dc/terms/identifier | "doi:10.4049/jimmunol.1101771"xsd:string |
| http://purl.uniprot.org/citations/22250081 | http://purl.uniprot.org/core/author | "Holmgren J."xsd:string |
| http://purl.uniprot.org/citations/22250081 | http://purl.uniprot.org/core/author | "Czerkinsky C."xsd:string |
| http://purl.uniprot.org/citations/22250081 | http://purl.uniprot.org/core/author | "Sun J.B."xsd:string |
| http://purl.uniprot.org/citations/22250081 | http://purl.uniprot.org/core/date | "2012"xsd:gYear |
| http://purl.uniprot.org/citations/22250081 | http://purl.uniprot.org/core/name | "J Immunol"xsd:string |
| http://purl.uniprot.org/citations/22250081 | http://purl.uniprot.org/core/pages | "1686-1697"xsd:string |
| http://purl.uniprot.org/citations/22250081 | http://purl.uniprot.org/core/title | "B lymphocytes treated in vitro with antigen coupled to cholera toxin B subunit induce antigen-specific Foxp3(+) regulatory T cells and protect against experimental autoimmune encephalomyelitis."xsd:string |
| http://purl.uniprot.org/citations/22250081 | http://purl.uniprot.org/core/volume | "188"xsd:string |
| http://purl.uniprot.org/citations/22250081 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/22250081 |
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