pubmed-article:12705853 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:12705853 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
pubmed-article:12705853 | lifeskim:mentions | umls-concept:C0015744 | lld:lifeskim |
pubmed-article:12705853 | lifeskim:mentions | umls-concept:C2911691 | lld:lifeskim |
pubmed-article:12705853 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
pubmed-article:12705853 | pubmed:issue | 4 | lld:pubmed |
pubmed-article:12705853 | pubmed:dateCreated | 2003-4-22 | lld:pubmed |
pubmed-article:12705853 | pubmed:abstractText | MHC class I-restricted antigen presentation is an essential step in the priming of CD8 T lymphocytes during immune responses to infection. While microbial growth and clearance have been accurately measured in mammalian hosts, the duration of functional antigen presentation during infection remains undefined in vivo. Herein we characterize the activation of naive and memory T cells at different times during bacterial infection. Surprisingly, the host's ability to prime T cells is of much shorter duration than bacterial infection, inversely correlating with the development of pathogen-specific cytolytic T lymphocytes. Our studies demonstrate a feedback mechanism that limits the duration of effective in vivo antigen presentation, thereby modulating T cell responses by temporally restricting recruitment of naive T cells into the immune response. | lld:pubmed |
pubmed-article:12705853 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12705853 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12705853 | pubmed:language | eng | lld:pubmed |
pubmed-article:12705853 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12705853 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:12705853 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:12705853 | pubmed:month | Apr | lld:pubmed |
pubmed-article:12705853 | pubmed:issn | 1074-7613 | lld:pubmed |
pubmed-article:12705853 | pubmed:author | pubmed-author:PamerEric GEG | lld:pubmed |
pubmed-article:12705853 | pubmed:author | pubmed-author:WongPhillipP | lld:pubmed |
pubmed-article:12705853 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:12705853 | pubmed:volume | 18 | lld:pubmed |
pubmed-article:12705853 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:12705853 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:12705853 | pubmed:pagination | 499-511 | lld:pubmed |
pubmed-article:12705853 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
pubmed-article:12705853 | pubmed:meshHeading | pubmed-meshheading:12705853... | lld:pubmed |
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pubmed-article:12705853 | pubmed:meshHeading | pubmed-meshheading:12705853... | lld:pubmed |
pubmed-article:12705853 | pubmed:year | 2003 | lld:pubmed |
pubmed-article:12705853 | pubmed:articleTitle | Feedback regulation of pathogen-specific T cell priming. | lld:pubmed |
pubmed-article:12705853 | pubmed:affiliation | Infectious Diseases Service, Department of Medicine, Immunology Program, Sloan-Kettering Institute, Memorial Sloan-Kettering Cancer Center, New York, NY 10021, USA. | lld:pubmed |
pubmed-article:12705853 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:12705853 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:12705853 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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