| pubmed-article:18222733 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18222733 | lifeskim:mentions | umls-concept:C0001811 | lld:lifeskim |
| pubmed-article:18222733 | lifeskim:mentions | umls-concept:C0012655 | lld:lifeskim |
| pubmed-article:18222733 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
| pubmed-article:18222733 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:18222733 | pubmed:dateCreated | 2008-3-18 | lld:pubmed |
| pubmed-article:18222733 | pubmed:abstractText | With increasing age, the competence of the immune system to fight infections and tumors declines. Age-dependent changes have been mostly described for human CD8 T cells, raising the question of whether the response patterns for CD4 T cells are different. Gene expression arrays of memory CD4 T cells yielded a similar age-induced fingerprint as has been described for CD8 T cells. In cross-sectional studies, the phenotypic changes were not qualitatively different for CD4 and CD8 T cells, but occurred much more frequently in CD8 T cells. Homeostatic stability partially explained this lesser age sensitivity of CD4 T cells. With aging, naïve and central memory CD8 T cells were lost at the expense of phenotypically distinct CD8 effector T cells, while effector CD4 T cells did not accumulate. However, phenotypic shifts on central memory T cells were also more pronounced in CD8 T cells. This distinct stability in cell surface marker expression can be reproduced in vitro. The data show that CD8 T cells are age sensitive by at least two partially independent mechanisms: fragile homeostatic control and gene expression instability in a large set of regulatory cell surface molecules. | lld:pubmed |
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| pubmed-article:18222733 | pubmed:language | eng | lld:pubmed |
| pubmed-article:18222733 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18222733 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:18222733 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18222733 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:18222733 | pubmed:issn | 1521-6616 | lld:pubmed |
| pubmed-article:18222733 | pubmed:author | pubmed-author:OuslanderJose... | lld:pubmed |
| pubmed-article:18222733 | pubmed:author | pubmed-author:WeyandCorneli... | lld:pubmed |
| pubmed-article:18222733 | pubmed:author | pubmed-author:GoronzyJörg... | lld:pubmed |
| pubmed-article:18222733 | pubmed:author | pubmed-author:LeeWon-WooWW | lld:pubmed |
| pubmed-article:18222733 | pubmed:author | pubmed-author:YangZhi-Zhang... | lld:pubmed |
| pubmed-article:18222733 | pubmed:author | pubmed-author:HirumaYukoY | lld:pubmed |
| pubmed-article:18222733 | pubmed:author | pubmed-author:LamarDavid... | lld:pubmed |
| pubmed-article:18222733 | pubmed:author | pubmed-author:CuiDapengD | lld:pubmed |
| pubmed-article:18222733 | pubmed:author | pubmed-author:Czesnikiewicz... | lld:pubmed |
| pubmed-article:18222733 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:18222733 | pubmed:volume | 127 | lld:pubmed |
| pubmed-article:18222733 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:18222733 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:18222733 | pubmed:pagination | 107-18 | lld:pubmed |
| pubmed-article:18222733 | pubmed:dateRevised | 2010-12-3 | lld:pubmed |
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| pubmed-article:18222733 | pubmed:year | 2008 | lld:pubmed |
| pubmed-article:18222733 | pubmed:articleTitle | T cell subset-specific susceptibility to aging. | lld:pubmed |
| pubmed-article:18222733 | pubmed:affiliation | Kathleen B. and Mason I. Lowance Center for Human Immunology, Emory University School of Medicine, Atlanta, GA30322, USA. | lld:pubmed |
| pubmed-article:18222733 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:18222733 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:18222733 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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