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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1999-6-22
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0270-9139
pubmed:author
pubmed:issnType
Print
pubmed:volume
29
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1799-808
pubmed:dateRevised
2008-11-21
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
pubmed:year
1999
pubmed:articleTitle
The roles of intrahepatic Valpha14(+) NK1.1(+) T cells for liver injury induced by Salmonella infection in mice.
pubmed:affiliation
Laboratory of Host Defense and Germfree Life, Research Institute for Disease Mechanism and Control, Nagoya, Japan.
pubmed:publicationType
Journal Article