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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
11
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pubmed:dateCreated |
2003-10-20
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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.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD44,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD45,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD95,
http://linkedlifedata.com/resource/pubmed/chemical/Chromatin,
http://linkedlifedata.com/resource/pubmed/chemical/DNA, Single-Stranded,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoglobulin G,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoglobulin M,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-2,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Proteins
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0953-8178
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
15
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1327-40
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:14565931-Animals,
pubmed-meshheading:14565931-Antigens, CD44,
pubmed-meshheading:14565931-Antigens, CD45,
pubmed-meshheading:14565931-Antigens, CD95,
pubmed-meshheading:14565931-Apoptosis,
pubmed-meshheading:14565931-Autoimmune Diseases,
pubmed-meshheading:14565931-B-Lymphocytes,
pubmed-meshheading:14565931-Chromatin,
pubmed-meshheading:14565931-DNA, Single-Stranded,
pubmed-meshheading:14565931-Female,
pubmed-meshheading:14565931-Immunoglobulin G,
pubmed-meshheading:14565931-Immunoglobulin M,
pubmed-meshheading:14565931-Interleukin-2,
pubmed-meshheading:14565931-Lymph Nodes,
pubmed-meshheading:14565931-Lymphatic Diseases,
pubmed-meshheading:14565931-Lymphoproliferative Disorders,
pubmed-meshheading:14565931-Mice,
pubmed-meshheading:14565931-Mice, Knockout,
pubmed-meshheading:14565931-Recombinant Proteins,
pubmed-meshheading:14565931-Spleen,
pubmed-meshheading:14565931-Thymus Gland
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pubmed:year |
2003
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pubmed:articleTitle |
Combined deficiency in CD44 and Fas leads to exacerbation of lymphoproliferative and autoimmune disease.
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pubmed:affiliation |
Department of Microbiology and Immunology, Medical College of Virginia Campus, Virginia Commonwealth University, Richmond, VA 23298, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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