pubmed-article:14565931 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:14565931 | lifeskim:mentions | umls-concept:C0004364 | lld:lifeskim |
pubmed-article:14565931 | lifeskim:mentions | umls-concept:C1332712 | lld:lifeskim |
pubmed-article:14565931 | lifeskim:mentions | umls-concept:C0011155 | lld:lifeskim |
pubmed-article:14565931 | lifeskim:mentions | umls-concept:C1539477 | lld:lifeskim |
pubmed-article:14565931 | lifeskim:mentions | umls-concept:C0205195 | lld:lifeskim |
pubmed-article:14565931 | lifeskim:mentions | umls-concept:C0181586 | lld:lifeskim |
pubmed-article:14565931 | pubmed:issue | 11 | lld:pubmed |
pubmed-article:14565931 | pubmed:dateCreated | 2003-10-20 | lld:pubmed |
pubmed-article:14565931 | pubmed:abstractText | Patients with mutations in Fas develop autoimmune lymphoproliferative disease (ALPS), while their family members with similar mutations are often normal, thereby suggesting that additional factors may play a role in the development of ALPS. In the current study, we tested the role of CD44 in the development of lymphoproliferative disease by generating CD44(-/-)/Fas(-/-) mice, which failed to express CD44 and Fas, and compared them to CD44(+/+)/Fas(-/-) mice that expressed CD44, but not Fas. The results showed that CD44(-/-)/Fas(-/-) mice developed a more severe lymphoproliferative and autoimmune disease when compared to CD44(+/+)/Fas(-/-) mice. This was indicated by increased numbers of cells in their lymph nodes, and a greater proportion of B220(+)CD4(-)CD8(-) (double-negative) T cells as well as antibodies against single-stranded DNA and chromatin. The heightened severity of lymphoproliferative disease seen in CD44(-/-)/Fas(-/-) mice correlated with increased resistance of T cells, but not B cells, to undergo activation-induced cell death (AICD). The current study suggests that deficiency in CD44 in combination with a defect in one of the molecules involved in the death receptor family such as Fas can further down-regulate AICD, and exacerbate the lymphoproliferative and autoimmune disease. | lld:pubmed |
pubmed-article:14565931 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:14565931 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:14565931 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:14565931 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:14565931 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:14565931 | pubmed:language | eng | lld:pubmed |
pubmed-article:14565931 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:14565931 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:14565931 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:14565931 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:14565931 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:14565931 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:14565931 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:14565931 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:14565931 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:14565931 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:14565931 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:14565931 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:14565931 | pubmed:month | Nov | lld:pubmed |
pubmed-article:14565931 | pubmed:issn | 0953-8178 | lld:pubmed |
pubmed-article:14565931 | pubmed:author | pubmed-author:McKallipRober... | lld:pubmed |
pubmed-article:14565931 | pubmed:author | pubmed-author:NagarkattiPra... | lld:pubmed |
pubmed-article:14565931 | pubmed:author | pubmed-author:NagarkattiMit... | lld:pubmed |
pubmed-article:14565931 | pubmed:author | pubmed-author:DoYoonkyungY | lld:pubmed |
pubmed-article:14565931 | pubmed:author | pubmed-author:Rafi-Janajreh... | lld:pubmed |
pubmed-article:14565931 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:14565931 | pubmed:volume | 15 | lld:pubmed |
pubmed-article:14565931 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:14565931 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:14565931 | pubmed:pagination | 1327-40 | lld:pubmed |
pubmed-article:14565931 | pubmed:dateRevised | 2007-11-15 | lld:pubmed |
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pubmed-article:14565931 | pubmed:year | 2003 | lld:pubmed |
pubmed-article:14565931 | pubmed:articleTitle | Combined deficiency in CD44 and Fas leads to exacerbation of lymphoproliferative and autoimmune disease. | lld:pubmed |
pubmed-article:14565931 | pubmed:affiliation | Department of Microbiology and Immunology, Medical College of Virginia Campus, Virginia Commonwealth University, Richmond, VA 23298, USA. | lld:pubmed |
pubmed-article:14565931 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:14565931 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
entrez-gene:12505 | entrezgene:pubmed | pubmed-article:14565931 | lld:entrezgene |
entrez-gene:14102 | entrezgene:pubmed | pubmed-article:14565931 | lld:entrezgene |