| http://purl.uniprot.org/citations/16887989 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/16887989 | http://www.w3.org/2000/01/rdf-schema#comment | "Lat(Y136F) knock-in mice harbor a point mutation in Tyr(136) of the linker for activation of T cells and show accumulation of Th2 effector cells and IgG1 and IgE hypergammaglobulinemia. B cell activation is not a direct effect of the mutation on B cells since in the absence of T cells, mutant B cells do not show an activated phenotype. After adoptive transfer of linker for activation of T cell mutant T cells into wild-type, T cell-deficient recipients, recipient B cells become activated. We show in vivo and in vitro that the Lat(Y136F) mutation promotes T cell-dependent B cell activation leading to germinal center, memory, and plasma cell formation even in an MHC class II-independent manner. All the plasma and memory B cell populations found in physiological T cell-dependent B cell responses are found. Characterization of the abundant plasmablasts found in secondary lymphoid organs of Lat(Y136F) mice revealed the presence of a previously uncharacterized CD93-expressing subpopulation, whose presence was confirmed in wild-type mice after immunization. In Lat(Y136F) mice, B cell activation was polyclonal and not Ag-driven because the increase in serum IgG1 and IgE concentrations involved Abs and autoantibodies with different specificities equally. Although the noncomplement-fixing IgG1 and IgE are the only isotypes significantly increased in Lat(Y136F) serum, we observed early-onset systemic autoimmunity with nephritis showing IgE autoantibody deposits and severe proteinuria. These results show that Th2 cells developing in Lat(Y136F) mice can trigger polyclonal B cell activation and thereby lead to systemic autoimmune disease."xsd:string |
| http://purl.uniprot.org/citations/16887989 | http://purl.org/dc/terms/identifier | "doi:10.4049/jimmunol.177.4.2285"xsd:string |
| http://purl.uniprot.org/citations/16887989 | http://purl.uniprot.org/core/author | "Wang Y."xsd:string |
| http://purl.uniprot.org/citations/16887989 | http://purl.uniprot.org/core/author | "Izui S."xsd:string |
| http://purl.uniprot.org/citations/16887989 | http://purl.uniprot.org/core/author | "Malissen B."xsd:string |
| http://purl.uniprot.org/citations/16887989 | http://purl.uniprot.org/core/author | "Malissen M."xsd:string |
| http://purl.uniprot.org/citations/16887989 | http://purl.uniprot.org/core/author | "Acha-Orbea H."xsd:string |
| http://purl.uniprot.org/citations/16887989 | http://purl.uniprot.org/core/author | "Delsol G."xsd:string |
| http://purl.uniprot.org/citations/16887989 | http://purl.uniprot.org/core/author | "Fournie G.J."xsd:string |
| http://purl.uniprot.org/citations/16887989 | http://purl.uniprot.org/core/author | "Genton C."xsd:string |
| http://purl.uniprot.org/citations/16887989 | http://purl.uniprot.org/core/date | "2006"xsd:gYear |
| http://purl.uniprot.org/citations/16887989 | http://purl.uniprot.org/core/name | "J Immunol"xsd:string |
| http://purl.uniprot.org/citations/16887989 | http://purl.uniprot.org/core/pages | "2285-2293"xsd:string |
| http://purl.uniprot.org/citations/16887989 | http://purl.uniprot.org/core/title | "The Th2 lymphoproliferation developing in LatY136F mutant mice triggers polyclonal B cell activation and systemic autoimmunity."xsd:string |
| http://purl.uniprot.org/citations/16887989 | http://purl.uniprot.org/core/volume | "177"xsd:string |
| http://purl.uniprot.org/citations/16887989 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/16887989 |
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