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rdf:type |
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lifeskim:mentions |
umls-concept:C0007603,
umls-concept:C0021467,
umls-concept:C0021469,
umls-concept:C0023745,
umls-concept:C0026336,
umls-concept:C0039194,
umls-concept:C0162638,
umls-concept:C0542341,
umls-concept:C0591833,
umls-concept:C0596761,
umls-concept:C0868945,
umls-concept:C1167250,
umls-concept:C1522424
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pubmed:issue |
1
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pubmed:dateCreated |
2004-4-20
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pubmed:abstractText |
We previously developed a transgenic mouse line into which a rabbit protein kinase Calpha (PKCalpha) gene fused to a human CD2 promoter/enhancer was introduced, and we found that immunosenescence was facilitated in these transgenic mice. In this study, we found that along with age-dependent increase in the level of protein expression of PKCalpha and its translocation to the membrane, activated T cells became less sensitive to apoptosis-inducing anti-Fas antibody. The capacity of T cells to express Fas antigen on their surfaces in response to anti-CD3 and interleukin-2 was impaired in PKCalpha-transgenic mice of relatively advanced age, although background Fas expression levels on T cells from those mice were high. We then found that out of proportion to a high level of cell surface Fas expression the density of cholera toxin B (CTx)-binding raft elements decreased in PKCalpha-transgenic mice of relatively advanced age and to a lesser extent in normal mice of advanced age. Correspondingly, the expression level of raft-associating Lck was decreased in these mice. These findings suggest for the first time that immunosenescence of T cells involves a decrease in density of cell surface CTx-binding raft elements, which might underlie a deterioration in T-cell signal pathway for either cell death or cell activation.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/15096185-10336426,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15096185-10363787,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15096185-10464309,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15096185-10525547,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15096185-10528172,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15096185-10576607,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15096185-10723795,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15096185-10963436,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15096185-11035063,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15096185-11549733,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15096185-11739199,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15096185-11751579,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15096185-11818332,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15096185-12359234,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15096185-12499387,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15096185-1382058,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15096185-1678398,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15096185-2137095,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15096185-2564317,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15096185-6216113,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15096185-7533498,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15096185-7688515,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15096185-8089201,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15096185-8347297,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15096185-9209497,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15096185-9255758,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15096185-9278292,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15096185-9310840,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15096185-9431985,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15096185-9606992,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15096185-9655486,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15096185-9701026,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15096185-9720650,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15096185-9729044,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15096185-9821870
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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 |
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0019-2805
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
112
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
64-71
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:15096185-Aging,
pubmed-meshheading:15096185-Animals,
pubmed-meshheading:15096185-Antigens, CD95,
pubmed-meshheading:15096185-Apoptosis,
pubmed-meshheading:15096185-Cells, Cultured,
pubmed-meshheading:15096185-Cholera Toxin,
pubmed-meshheading:15096185-Disease Models, Animal,
pubmed-meshheading:15096185-Immune Tolerance,
pubmed-meshheading:15096185-Interleukin-2,
pubmed-meshheading:15096185-Lymphocyte Activation,
pubmed-meshheading:15096185-Membrane Microdomains,
pubmed-meshheading:15096185-Mice,
pubmed-meshheading:15096185-Mice, Transgenic,
pubmed-meshheading:15096185-Protein Kinase C,
pubmed-meshheading:15096185-Protein Kinase C-alpha,
pubmed-meshheading:15096185-Signal Transduction,
pubmed-meshheading:15096185-T-Lymphocytes
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pubmed:year |
2004
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pubmed:articleTitle |
Inhibition of Fas-mediated apoptotic cell death of murine T lymphocytes in a mouse model of immunosenescence in linkage to deterioration in cell membrane raft function.
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pubmed:affiliation |
Department of Immunology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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