| http://purl.uniprot.org/citations/15905540 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/15905540 | http://www.w3.org/2000/01/rdf-schema#comment | "Complement receptor type 2 (CR2/CD21), in association with CD19, plays an important role in enhancing mature B cell responses to opsonized Ags. We have shown that mice expressing a human CR2/CD21 (hCR2/CD21) transgene during the CD43(+)/CD25(-) late pro-B cell stage of B cell development demonstrate marked changes in subsequent B cell ontogeny. In the present study, we show that the humoral immune response to the T cell-dependent Ag, sheep RBC, is muted severely in a manner inversely proportional to B cell expression level of hCR2. Individual Ag-specific IgG isotypes vary in the degree to which they are affected but all are reduced while IgM titers are normal. A substantial reduction in germinal centers, both in size and frequency, in the spleens of immunized hCR2 transgenic mice demonstrates a failure to maintain germinal center reaction. However, both IgM expression levels and LPS-proliferative responses appear fully intact in B cells from hCR2-positive mice, suggesting that this alteration in B cell phenotype is different qualitatively from that of specific Ag-defined anergy models. These data suggest that the unresponsiveness to T-dependent Ags displayed by hCR2-positive B cells is linked to an increase in the level of stimulus required to propel the B cell into a fully activated state and thus a normal humoral immune response to Ags. We conclude that this phenotype and these mice may offer an additional means to dissect mechanisms underlying B cell tolerance and Ag responsiveness both in bone marrow and periphery."xsd:string |
| http://purl.uniprot.org/citations/15905540 | http://purl.org/dc/terms/identifier | "doi:10.4049/jimmunol.174.11.6974"xsd:string |
| http://purl.uniprot.org/citations/15905540 | http://purl.uniprot.org/core/author | "Morgan B.P."xsd:string |
| http://purl.uniprot.org/citations/15905540 | http://purl.uniprot.org/core/author | "Holers V.M."xsd:string |
| http://purl.uniprot.org/citations/15905540 | http://purl.uniprot.org/core/author | "Marchbank K.J."xsd:string |
| http://purl.uniprot.org/citations/15905540 | http://purl.uniprot.org/core/author | "Kulik L."xsd:string |
| http://purl.uniprot.org/citations/15905540 | http://purl.uniprot.org/core/author | "Birrell L."xsd:string |
| http://purl.uniprot.org/citations/15905540 | http://purl.uniprot.org/core/date | "2005"xsd:gYear |
| http://purl.uniprot.org/citations/15905540 | http://purl.uniprot.org/core/name | "J Immunol"xsd:string |
| http://purl.uniprot.org/citations/15905540 | http://purl.uniprot.org/core/pages | "6974-6982"xsd:string |
| http://purl.uniprot.org/citations/15905540 | http://purl.uniprot.org/core/title | "B cells from mice prematurely expressing human complement receptor type 2 are unresponsive to T-dependent antigens."xsd:string |
| http://purl.uniprot.org/citations/15905540 | http://purl.uniprot.org/core/volume | "174"xsd:string |
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