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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
8
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pubmed:dateCreated |
1999-5-6
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pubmed:abstractText |
In animals, T cells often die rapidly after activation, unless activation occurs in the presence of inflammatory factors. To understand how such activated cells survive to participate in immune responses, we studied the effects of viral infection on T cells responding to an unrelated superantigen. Normal T cells activated by superantigen in uninfected mice died as a result of their activation, whereas T cells that were activated during vaccinia infection survived longer in vivo and in culture. This bystander effect of viral infection on activated T cells was independent of effects on the magnitude of the initial T cell response, on induction of Bcl-2 and Bcl-x, on T cell proliferation, and on Fas killing. The failure of such effects to predict the fate of activated T cells in vivo indicates that virus infections shape T cell responses via mechanisms that differ from those described previously. These mechanisms may contribute to the ability of viral infections to induce autoimmunity.
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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 |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD95,
http://linkedlifedata.com/resource/pubmed/chemical/Bcl2l1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Enterotoxins,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-bcl-2,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Antigen, T-Cell...,
http://linkedlifedata.com/resource/pubmed/chemical/Superantigens,
http://linkedlifedata.com/resource/pubmed/chemical/bcl-X Protein,
http://linkedlifedata.com/resource/pubmed/chemical/enterotoxin A, Staphylococcal
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
0022-1767
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
162
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
4527-35
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:10201991-Animals,
pubmed-meshheading:10201991-Antigens, CD95,
pubmed-meshheading:10201991-CD4-Positive T-Lymphocytes,
pubmed-meshheading:10201991-Cell Death,
pubmed-meshheading:10201991-Cell Survival,
pubmed-meshheading:10201991-Cells, Cultured,
pubmed-meshheading:10201991-Cytokines,
pubmed-meshheading:10201991-Enterotoxins,
pubmed-meshheading:10201991-Female,
pubmed-meshheading:10201991-Lymph Nodes,
pubmed-meshheading:10201991-Lymphocyte Activation,
pubmed-meshheading:10201991-Mice,
pubmed-meshheading:10201991-Mice, Inbred C57BL,
pubmed-meshheading:10201991-Proto-Oncogene Proteins c-bcl-2,
pubmed-meshheading:10201991-Receptors, Antigen, T-Cell, alpha-beta,
pubmed-meshheading:10201991-Staphylococcus aureus,
pubmed-meshheading:10201991-Superantigens,
pubmed-meshheading:10201991-T-Lymphocyte Subsets,
pubmed-meshheading:10201991-Time Factors,
pubmed-meshheading:10201991-Transcription, Genetic,
pubmed-meshheading:10201991-Vaccinia,
pubmed-meshheading:10201991-bcl-X Protein
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pubmed:year |
1999
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pubmed:articleTitle |
Bystander virus infection prolongs activated T cell survival.
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pubmed:affiliation |
Department of Medicine, National Jewish Medical and Research Center, Howard Hughes Medical Institute, Denver, CO 80206, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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