| pubmed-article:11602643 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11602643 | lifeskim:mentions | umls-concept:C0005953 | lld:lifeskim |
| pubmed-article:11602643 | lifeskim:mentions | umls-concept:C0004561 | lld:lifeskim |
| pubmed-article:11602643 | lifeskim:mentions | umls-concept:C0332197 | lld:lifeskim |
| pubmed-article:11602643 | lifeskim:mentions | umls-concept:C0019868 | lld:lifeskim |
| pubmed-article:11602643 | lifeskim:mentions | umls-concept:C0205100 | lld:lifeskim |
| pubmed-article:11602643 | pubmed:issue | 8 | lld:pubmed |
| pubmed-article:11602643 | pubmed:dateCreated | 2001-10-16 | lld:pubmed |
| pubmed-article:11602643 | pubmed:abstractText | To study homeostasis of peripheral B lymphocytes in the absence of B cell influx from the bone marrow, we generated a mouse mutant in which the recombination-activating gene (RAG)-2 can be inducibly deleted. When RAG-2 was deleted at the age of 8-10 wk, splenic naive follicular B cells were gradually lost over a year of observation, with a half-life of approximately 4.5 mo. By contrast, the pool of marginal zone B cells in the spleen and of B-1 cells in the peritoneal cavity were kept at normal level. In lymph nodes, approximately 90% of the B cells were lost within 4 mo, and B cell numbers remained constant thereafter. Mice in which RAG-2 was deleted at birth maintained a small population of activated B cells with an increased proportion of marginal zone B cells. Additionally, an increase of the pool of IgM secreting cells and B-1a cells was observed. | lld:pubmed |
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| pubmed-article:11602643 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11602643 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11602643 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:11602643 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11602643 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:11602643 | pubmed:issn | 0022-1007 | lld:pubmed |
| pubmed-article:11602643 | pubmed:author | pubmed-author:RajewskyKK | lld:pubmed |
| pubmed-article:11602643 | pubmed:author | pubmed-author:HauPP | lld:pubmed |
| pubmed-article:11602643 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11602643 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:11602643 | pubmed:volume | 194 | lld:pubmed |
| pubmed-article:11602643 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11602643 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11602643 | pubmed:pagination | 1151-64 | lld:pubmed |
| pubmed-article:11602643 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:11602643 | pubmed:year | 2001 | lld:pubmed |
| pubmed-article:11602643 | pubmed:articleTitle | Homeostasis of peripheral B cells in the absence of B cell influx from the bone marrow. | lld:pubmed |
| pubmed-article:11602643 | pubmed:affiliation | Department of Immunology, Institute for Genetics, University of Cologne, D-50931 Cologne, Germany. | lld:pubmed |
| pubmed-article:11602643 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11602643 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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