rdf:type |
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lifeskim:mentions |
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pubmed:issue |
3
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pubmed:dateCreated |
1984-6-25
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pubmed:abstractText |
To examine the lysis of virus-infected cells in vivo, uninfected and lymphocytic choriomeningitis virus (LCMV)-infected L-929 cells were labeled in vitro with [125I]-iododeoxyuridine and implanted intravenously into mice. Natural cytotoxicity against both uninfected and virus-infected cells was demonstrated in normal uninfected mice, but LCMV-infected cells were cleared from the lungs and whole bodies more rapidly than uninfected cells. Treatment of L-929 cells with defective interfering LCMV inhibited standard virus synthesis and protected the target cells from enhanced in vivo rejection. The in vivo rejection was apparently mediated by a cellular constituent of the host immune response and not simply a result of virus-induced cytopathic effects on the target cell, as hydrocortisone acetate and cyclophosphamide each reduced rejection of both target cell types and eliminated the enhanced rejection of LCMV-infected cells. The enhanced rejection of LCMV-infected cells was not restricted by histocompatibility antigens, indicating that classic T-cell recognition was not involved in the lysis, and since the enhanced rejection of LCMV-infected cells was mediated by mice treated with cobra venom factor, complement was also not involved in the lysis. Although moderate levels of interferon (102 U/ml) were present in the sera and although there was a modest activation of natural killer (NK) cells in the lungs of LCMV-infected cell recipients but not uninfected cell recipients, the enhanced rejection of virus-infected cells did not appear to be NK cell mediated. Normal mice and mice depleted of NK cell activity by in vivo treatment with antibody to asialo ganglio-n-tetraosylceramide ( AGM1 ) rejected uninfected and LCMV-infected L-929 cells similarly. This antibody markedly inhibited the rejection of NK-sensitive YAC-1 cells. In addition to the natural cytotoxicity directed against virus-infected cells, a second nonspecific rejection mechanism appeared in response to treatment protocols which induced interferon. Polyinosinic-polycytidylic acid and infection with LCMV augmented in vivo rejection of both uninfected and LCMV-infected L-929 cells but eliminated the differential rejection of the virus-infected cells. Infection with LCMV also augmented the in vivo rejection of the NK-sensitive target cell, YAC-1. In vivo treatments with anti- AGM1 sera only moderately inhibited the elevated rejection of uninfected and LCMV-infected L-929 cells, indicating that the enhanced rejection of these target cells was predominantly mediated by a mechanism other than that mediated by NK cells.(ABSTRACT TRUNCATED AT 400 WORDS)
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/6374165-1234049,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6374165-150448,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6374165-221611,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6374165-280711,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6374165-301173,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6374165-302419,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6374165-307587,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6374165-310826,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6374165-334980,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6374165-380148,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6374165-4622135,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6374165-480377,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6374165-6154106,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6374165-6154658,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/6374165-6244358,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6374165-6309965,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6374165-6403648,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/6374165-956654
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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 |
Jun
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pubmed:issn |
0022-538X
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
50
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
698-707
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:6374165-Animals,
pubmed-meshheading:6374165-Cell Line,
pubmed-meshheading:6374165-Complement System Proteins,
pubmed-meshheading:6374165-Cyclophosphamide,
pubmed-meshheading:6374165-Fluorescent Antibody Technique,
pubmed-meshheading:6374165-Hydrocortisone,
pubmed-meshheading:6374165-Immunity, Innate,
pubmed-meshheading:6374165-Killer Cells, Natural,
pubmed-meshheading:6374165-L Cells (Cell Line),
pubmed-meshheading:6374165-Leukemia, Experimental,
pubmed-meshheading:6374165-Lymphocytic choriomeningitis virus,
pubmed-meshheading:6374165-Mice,
pubmed-meshheading:6374165-Mice, Inbred C57BL,
pubmed-meshheading:6374165-Mice, Inbred Strains
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pubmed:year |
1984
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pubmed:articleTitle |
Lysis of uninfected and virus-infected cells in vivo: a rejection mechanism in addition to that mediated by natural killer cells.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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