Source:http://linkedlifedata.com/resource/pubmed/id/17823982
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rdf:type | |
lifeskim:mentions |
umls-concept:C0021311,
umls-concept:C0030664,
umls-concept:C0039194,
umls-concept:C0040300,
umls-concept:C0040690,
umls-concept:C0041221,
umls-concept:C0085358,
umls-concept:C0277785,
umls-concept:C0851285,
umls-concept:C1332717,
umls-concept:C1413244,
umls-concept:C1517004,
umls-concept:C1706438,
umls-concept:C2698600
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pubmed:issue |
10
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pubmed:dateCreated |
2007-10-2
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pubmed:abstractText |
Infection with the protozoan parasite Trypanosoma cruzi leads to chronic infection, with parasite persistence primarily in muscle tissue. CD8(+) T cells isolated from muscle tissue of T. cruzi-infected mice display decreased production of IFN-gamma in response to T cell receptor engagement. The expression of TGF-beta at the site of CD8(+) T cell dysfunction and parasite persistence suggested that this immunoregulatory cytokine might play a role in these processes. Mice expressing a T cell-specific dominant negative TGF-beta receptor type II (DNRII) were therefore infected with T. cruzi. Infection of DNRII mice resulted in massive CD8(+) T cell proliferation, leading to increased numbers but decreased frequencies of antigen-specific CD8(+) T cells in the spleen compared to wild-type mice. However, TGF-beta unresponsiveness failed to restore effector functions of CD8(+) T cells isolated from muscle tissue. Histological examination of skeletal muscle from T. cruzi-infected DNRII mice revealed an extensive cellular infiltrate, and DNRII mice displayed higher susceptibility to infection. Overall, while TGF-beta does not appear to be responsible for CD8(+) T cell unresponsiveness in peripheral tissue in T. cruzi-infected mice, these data suggest a role for TGF-beta in control of immunopathology in response to T. cruzi infection.
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pubmed:grant | |
pubmed:commentsCorrections | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Protein-Serine-Threonine Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Transforming Growth...,
http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factor beta,
http://linkedlifedata.com/resource/pubmed/chemical/transforming growth factor-beta...
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
0014-2980
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
37
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2764-71
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pubmed:dateRevised |
2008-1-23
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pubmed:meshHeading |
pubmed-meshheading:17823982-Animals,
pubmed-meshheading:17823982-CD8-Positive T-Lymphocytes,
pubmed-meshheading:17823982-Cells, Cultured,
pubmed-meshheading:17823982-Chagas Disease,
pubmed-meshheading:17823982-Disease Models, Animal,
pubmed-meshheading:17823982-Mice,
pubmed-meshheading:17823982-Mice, Inbred C57BL,
pubmed-meshheading:17823982-Mice, Knockout,
pubmed-meshheading:17823982-Protein-Serine-Threonine Kinases,
pubmed-meshheading:17823982-Receptors, Transforming Growth Factor beta,
pubmed-meshheading:17823982-Transforming Growth Factor beta
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pubmed:year |
2007
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pubmed:articleTitle |
TGF-beta regulates pathology but not tissue CD8+ T cell dysfunction during experimental Trypanosoma cruzi infection.
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pubmed:affiliation |
Department of Cellular Biology and Center for Tropical and Emerging Global Diseases, University of Georgia, Athens, GA 30605, USA.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, N.I.H., Extramural
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