| pubmed-article:12853163 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12853163 | lifeskim:mentions | umls-concept:C0004561 | lld:lifeskim |
| pubmed-article:12853163 | lifeskim:mentions | umls-concept:C0007620 | lld:lifeskim |
| pubmed-article:12853163 | lifeskim:mentions | umls-concept:C1420816 | lld:lifeskim |
| pubmed-article:12853163 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:12853163 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:12853163 | pubmed:dateCreated | 2003-7-10 | lld:pubmed |
| pubmed-article:12853163 | pubmed:abstractText | The TNF family member BAFF is a fundamental survival factor for B cells. BAFF binds to three receptors, only one of which, BAFF-R, does not cross-react with the BAFF-related ligand APRIL. The survival function of BAFF on B cells is mediated mainly by BAFF-R and is particularly effective in transitional B cells. BAFF depletion leads to a considerable decrease in mature B cells, without apparent effect on B cell genesis. Consistently, BAFF overexpression results in an expanded B cell compartment and autoimmunity in mice. Elevated amounts of BAFF can be found in the serum of patients suffering from autoimmune diseases. The BAFF system is a promising target for the treatment of autoimmune diseases. | lld:pubmed |
| pubmed-article:12853163 | pubmed:language | eng | lld:pubmed |
| pubmed-article:12853163 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12853163 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:12853163 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12853163 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:12853163 | pubmed:issn | 0165-2478 | lld:pubmed |
| pubmed-article:12853163 | pubmed:author | pubmed-author:SchneiderPasc... | lld:pubmed |
| pubmed-article:12853163 | pubmed:author | pubmed-author:TschoppJürgJ | lld:pubmed |
| pubmed-article:12853163 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:12853163 | pubmed:day | 3 | lld:pubmed |
| pubmed-article:12853163 | pubmed:volume | 88 | lld:pubmed |
| pubmed-article:12853163 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12853163 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12853163 | pubmed:pagination | 57-62 | lld:pubmed |
| pubmed-article:12853163 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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| pubmed-article:12853163 | pubmed:meshHeading | pubmed-meshheading:12853163... | lld:pubmed |
| pubmed-article:12853163 | pubmed:year | 2003 | lld:pubmed |
| pubmed-article:12853163 | pubmed:articleTitle | BAFF and the regulation of B cell survival. | lld:pubmed |
| pubmed-article:12853163 | pubmed:affiliation | Institute of Biochemistry, BIL Biomedical Research Center, University of Lausanne, Ch. des Boveresses 155, CH-1066, Epalinges, Switzerland. | lld:pubmed |
| pubmed-article:12853163 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:12853163 | pubmed:publicationType | Review | lld:pubmed |
| pubmed-article:12853163 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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