Source:http://linkedlifedata.com/resource/pubmed/id/10347123
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
1999-6-22
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pubmed:abstractText |
To investigate the roles of intrahepatic T cells in liver injury after Salmonella infection, we examined serum alanine transaminase (ALT), histopathology, and bacterial numbers in liver after infection with Salmonella choleraesuis strain 31N-1 in mice genetically lacking TCRalpha beta+, CD4(+), CD8(+), or NK1.1(+)T cells with C57BL/6 background. In control (+/+) mice, serum ALT reached a peak level by day 7 after an intraperitoneal inoculation of 2 x 10(6) CFU Salmonella choleraesuis 31N-1. In TCR-beta-/- mice, liver injury, as assessed by serum ALT level and histological examination, was significantly suppressed on day 7 after Salmonella infection but the numbers of bacteria in liver did not differ from those in normal mice, suggesting that alpha beta T cells are responsible for liver injury induced by Salmonella infection. To further determine which subsets in alpha beta T cells are important for the liver injury, we compared serum ALT level in mice genetically lacking CD4, CD8, beta2-microglobulin (beta2m, IAbeta, or Jalpha281 after Salmonella infection. In CD4(-/-) mice, serum ALT was significantly lower in comparison with control mice, but there was no difference in serum ALT levels in CD8(-/-) and IAbeta-/- mice from that in control mice. Notably, serum ALT levels and pathological lesions in liver were significantly decreased in beta2m-/- or Jalpha281(-/-) mice, which lacked in NK1.1(+) T cells bearing TCR Valpha14-Jalpha281 specific for beta2m-associated CD1d, following Salmonella infection. Taken together, it is suggested that alpha beta T cells bearing NK1.1 and CD4 may be main effector cells for liver injury after Salmonella infection.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Alanine Transaminase,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD4,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD8,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Antigen, T-Cell...,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha,
http://linkedlifedata.com/resource/pubmed/chemical/beta 2-Microglobulin
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0270-9139
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
29
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1799-808
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:10347123-Alanine Transaminase,
pubmed-meshheading:10347123-Animals,
pubmed-meshheading:10347123-Antigens, CD4,
pubmed-meshheading:10347123-Antigens, CD8,
pubmed-meshheading:10347123-Female,
pubmed-meshheading:10347123-Flow Cytometry,
pubmed-meshheading:10347123-Genes, T-Cell Receptor beta,
pubmed-meshheading:10347123-Interferon-gamma,
pubmed-meshheading:10347123-Killer Cells, Natural,
pubmed-meshheading:10347123-Liver,
pubmed-meshheading:10347123-Male,
pubmed-meshheading:10347123-Mice,
pubmed-meshheading:10347123-Mice, Inbred C57BL,
pubmed-meshheading:10347123-Mice, Knockout,
pubmed-meshheading:10347123-Receptors, Antigen, T-Cell, alpha-beta,
pubmed-meshheading:10347123-Salmonella,
pubmed-meshheading:10347123-Salmonella Infections, Animal,
pubmed-meshheading:10347123-T-Lymphocyte Subsets,
pubmed-meshheading:10347123-Tumor Necrosis Factor-alpha,
pubmed-meshheading:10347123-beta 2-Microglobulin
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pubmed:year |
1999
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pubmed:articleTitle |
The roles of intrahepatic Valpha14(+) NK1.1(+) T cells for liver injury induced by Salmonella infection in mice.
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pubmed:affiliation |
Laboratory of Host Defense and Germfree Life, Research Institute for Disease Mechanism and Control, Nagoya, Japan.
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pubmed:publicationType |
Journal Article
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