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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
25
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pubmed:dateCreated |
1997-1-15
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pubmed:abstractText |
beta 2-Microglobulin-deficient (beta 2m-) mice generate a CD4+ major histocompatibility complex class II-restricted cytotoxic T-lymphocyte (CTL) response following infection with lymphocytic choriomeningitis (LCM) virus (LCMV). We have determined the cytotoxic mechanism used by these CD4+ CTLs and have examined the role of this cytotoxic activity in pathogenesis of LCM disease in beta 2m- mice. Lysis of LCMV-infected target cells by CTLs from beta 2m- mice is inhibited by addition of soluble Fas-Ig fusion proteins or by pretreatment of the CTLs with the protein synthesis inhibitor emetine. In addition, LCMV-infected cell lines that are resistant to anti-Fas-induced apoptosis are refractory to lysis by these virus-specific CD4+ CTLs. These data indicate that LCMV-specific CD4+ CTLs from beta 2m- mice use a Fas-dependent lytic mechanism. Intracranial (i.c.) infection of beta 2m- mice with LCMV results in loss of body weight. Fas-deficient beta 2m- Jpr mice develop a similar wasting disease following i.c. infection. This suggests that Fas-dependent cytotoxicity is not required for LCMV-induced weight loss. A potential mediator of this chronic wasting disease is tumor necrosis factor (TNF)-alpha, which is produced by LCMV-specific CD4+ CTLs. In contrast to LCMV-induced weight loss, lethal LCM disease in beta 2m- mice is dependent on Fas-mediated cytotoxicity. Transfer of immune splenocytes from LCMV-infected beta 2m- mice into irradiated infected beta 2m- mice results in death of recipient animals. In contrast, transfer of these splenocytes into irradiated infected beta 2m- Jpr mice does not cause death. Thus a role for CD4+ T-cell-mediated cytotoxicity in virus-induced immunopathology has now been demonstrated.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/8962123-1832087,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8962123-1839711,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8962123-2110460,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8962123-7477351,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8962123-7479970,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8962123-7493761,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8962123-7507960,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8962123-7514297,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8962123-7515183,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8962123-7518614,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8962123-7521365,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8962123-7530337,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8962123-7530760,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8962123-7537304,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8962123-7540783,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8962123-7882166,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8962123-7903551,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8962123-8093219,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8962123-8103060,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8962123-8164737,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8962123-8304235,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8962123-8396684,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8962123-8562499,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8962123-8598456,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8962123-8600538,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8962123-8676065,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8962123-8717513,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8962123-8786289,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8962123-8825286,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8962123-8961509
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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 |
Dec
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pubmed:issn |
0027-8424
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
10
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pubmed:volume |
93
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
14730-5
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:8962123-Adoptive Transfer,
pubmed-meshheading:8962123-Animals,
pubmed-meshheading:8962123-Antigens, CD95,
pubmed-meshheading:8962123-CD4-Positive T-Lymphocytes,
pubmed-meshheading:8962123-Cytotoxicity, Immunologic,
pubmed-meshheading:8962123-Humans,
pubmed-meshheading:8962123-Lymphocytic Choriomeningitis,
pubmed-meshheading:8962123-Mice,
pubmed-meshheading:8962123-beta 2-Microglobulin
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pubmed:year |
1996
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pubmed:articleTitle |
Fas-dependent CD4+ cytotoxic T-cell-mediated pathogenesis during virus infection.
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pubmed:affiliation |
Department of Microbiology and Immunology, University of North Carolina, Chapel Hill 27599, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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