Source:http://linkedlifedata.com/resource/pubmed/id/10843381
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5
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pubmed:dateCreated |
2000-6-20
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pubmed:abstractText |
The generation of an adaptive immune response against intracellular pathogens requires the recruitment of effector T cells to sites of infection. Here we show that the chemokine IP-10, a specific chemoattractant for activated T cells, controls this process in mice naturally infected with Toxoplasma gondii. Neutralization of IP-10 in infected mice inhibited the massive influx of T cells into tissues and impaired antigen-specific T cell effector functions. This resulted in >1000-fold increase in tissue parasite burden and a marked increase in mortality compared to control antibody-treated mice. These observations suggest that IP-10 may play a broader role in the localization and function of effector T cells at sites of Th1 inflammation.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
1074-7613
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
12
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
483-94
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:10843381-Animals,
pubmed-meshheading:10843381-Cell Movement,
pubmed-meshheading:10843381-Chemokine CXCL10,
pubmed-meshheading:10843381-Chemokines, CXC,
pubmed-meshheading:10843381-Chemotactic Factors,
pubmed-meshheading:10843381-Immunity, Innate,
pubmed-meshheading:10843381-Mice,
pubmed-meshheading:10843381-Mice, Inbred C57BL,
pubmed-meshheading:10843381-T-Lymphocytes,
pubmed-meshheading:10843381-Toxoplasma,
pubmed-meshheading:10843381-Toxoplasmosis, Animal
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pubmed:year |
2000
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pubmed:articleTitle |
IP-10 is critical for effector T cell trafficking and host survival in Toxoplasma gondii infection.
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pubmed:affiliation |
Department of Medicine, Dartmouth Medical Center, Hanover, New Hampshire 03755, USA.
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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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