Source:http://linkedlifedata.com/resource/pubmed/id/11160212
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
3
|
| pubmed:dateCreated |
2001-2-22
|
| pubmed:abstractText |
Previously, we observed that high-avidity CTL are much more effective in vivo than low-avidity CTL in elimination of infected cells, but the mechanisms behind their superior activity remained unclear. In this study, we identify two complementary mechanisms: 1) high-avidity CTL lyse infected cells earlier in the course of a viral infection by recognizing lower Ag densities than those distinguished by low-avidity CTL and 2) they initiate lysis of target cells more rapidly at any given Ag density. Alternative mechanisms were excluded, including: 1) the possibility that low-avidity CTL might control virus given more time (virus levels remained as high at 6 days following transfer as at 3 days) and 2) that differences in efficacy might be correlated with homing ability. Furthermore, adoptive transfer of high- and low-avidity CTL into SCID mice demonstrated that transfer of a 10-fold greater amount of low-avidity CTL could only partially compensate for their decreased ability to eliminate infected cells. Thus, we conclude that high-avidity CTL exploit two complementary mechanisms that combine to prevent the spread of virus within the animal: earlier recognition of infected cells when little viral protein has been made and more rapid lysis of infected cells.
|
| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
AIM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Feb
|
| pubmed:issn |
0022-1767
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:day |
1
|
| pubmed:volume |
166
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
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| pubmed:pagination |
1690-7
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| pubmed:dateRevised |
2006-11-15
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| pubmed:meshHeading |
pubmed-meshheading:11160212-Adoptive Transfer,
pubmed-meshheading:11160212-Animals,
pubmed-meshheading:11160212-Antigen Presentation,
pubmed-meshheading:11160212-Cell Line,
pubmed-meshheading:11160212-Cell Movement,
pubmed-meshheading:11160212-Clone Cells,
pubmed-meshheading:11160212-Cytotoxicity, Immunologic,
pubmed-meshheading:11160212-Cytotoxicity Tests, Immunologic,
pubmed-meshheading:11160212-Female,
pubmed-meshheading:11160212-HIV Antigens,
pubmed-meshheading:11160212-HIV Envelope Protein gp160,
pubmed-meshheading:11160212-Kinetics,
pubmed-meshheading:11160212-Mice,
pubmed-meshheading:11160212-Mice, Inbred BALB C,
pubmed-meshheading:11160212-Mice, Inbred DBA,
pubmed-meshheading:11160212-Mice, SCID,
pubmed-meshheading:11160212-Ovarian Diseases,
pubmed-meshheading:11160212-Peptide Fragments,
pubmed-meshheading:11160212-T-Lymphocyte Subsets,
pubmed-meshheading:11160212-T-Lymphocytes, Cytotoxic,
pubmed-meshheading:11160212-Tumor Cells, Cultured,
pubmed-meshheading:11160212-Vaccinia,
pubmed-meshheading:11160212-Vaccinia virus,
pubmed-meshheading:11160212-Viral Load
|
| pubmed:year |
2001
|
| pubmed:articleTitle |
High-avidity CTL exploit two complementary mechanisms to provide better protection against viral infection than low-avidity CTL.
|
| pubmed:affiliation |
Molecular Immunogenetics and Vaccine Research Section, Metabolism Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892-1578, USA.
|
| pubmed:publicationType |
Journal Article,
Comparative Study
|