Source:http://linkedlifedata.com/resource/pubmed/id/12244142
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
7
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pubmed:dateCreated |
2002-9-23
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pubmed:abstractText |
Complement receptor (CR) type 2 (CR2/CD21) is normally expressed only during the immature and mature stages of B cell development. In association with CD19, CR2 plays an important role in enhancing mature B cell responses to foreign Ag. We used a murine Vlambda2 promoter/Vlambda2-4 enhancer minigene to develop transgenic mice that initiate expression of human CR2 (hCR2) during the CD43(+)CD25(-) late pro-B cell stage of development. We found peripheral blood B cell numbers reduced by 60% in mice expressing high levels of hCR2 and by 15% in mice with intermediate receptor expression. Splenic B cell populations were altered with an expansion of marginal zone cells, and basal serum IgG levels as well as T-dependent immune responses were also significantly decreased in transgenic mice. Mice expressing the highest levels of hCR2 demonstrated in the bone marrow a slight increase in B220(int)CD43(+)CD25(-) B cells in association with a substantial decrease in immature and mature B cells, indicative of a developmental block in the pro-B cell stage. These data demonstrate that stage-specific expression of CR2 is necessary for normal B cell development, as premature receptor expression substantially alters this process. Alterations in B cell development are most likely due to engagement of pre-B cell receptor-mediated or other regulatory pathways by hCR2 in a CD19- and possibly C3 ligand-dependent manner.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
0022-1767
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
169
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
3526-35
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:12244142-Agammaglobulinemia,
pubmed-meshheading:12244142-Animals,
pubmed-meshheading:12244142-Antibody Formation,
pubmed-meshheading:12244142-B-Lymphocyte Subsets,
pubmed-meshheading:12244142-Cell Differentiation,
pubmed-meshheading:12244142-Crosses, Genetic,
pubmed-meshheading:12244142-Down-Regulation,
pubmed-meshheading:12244142-Humans,
pubmed-meshheading:12244142-Immunoglobulin G,
pubmed-meshheading:12244142-Immunophenotyping,
pubmed-meshheading:12244142-Lymphocyte Count,
pubmed-meshheading:12244142-Lymphopenia,
pubmed-meshheading:12244142-Mice,
pubmed-meshheading:12244142-Mice, Transgenic,
pubmed-meshheading:12244142-Organ Specificity,
pubmed-meshheading:12244142-Receptors, Complement 3d,
pubmed-meshheading:12244142-T-Lymphocyte Subsets
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pubmed:year |
2002
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pubmed:articleTitle |
Expression of human complement receptor type 2 (CD21) in mice during early B cell development results in a reduction in mature B cells and hypogammaglobulinemia.
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pubmed:affiliation |
Complement Biology Group, Department of Medical Biochemistry, University of Wales College of Medicine, Heath Park, Cardiff, United Kingdom.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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