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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
10
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pubmed:dateCreated |
2008-3-3
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pubmed:abstractText |
The obligate intracellular human pathogenic bacterium Chlamydia trachomatis has evolved multiple mechanisms to circumvent the host immune system. Infected cells exhibit a profound resistance to the induction of apoptosis and down-regulate the expression of major histocompatibility complex class I and class II molecules to evade the cytotoxic effect of effector immune cells. Here we demonstrate the down-regulation of tumor necrosis factor receptor 1 (TNFR1) on the surface of infected cells. Interestingly, other members of the TNFR family such as TNFR2 and CD95 (Fas/Apo-1) were not modulated during infection, suggesting a selective mechanism underlying surface reduction of TNFR1. The observed effect was not due to reduced expression since the overall amount of TNFR1 protein was increased in infected cells. TNFR1 accumulated at the chlamydial inclusion and was shed by the infected cell into the culture supernatant. Receptor shedding depended on the infection-induced activation of the MEK-ERK pathway and the metalloproteinase TACE (TNFalpha converting enzyme). Our results point to a new function of TNFR1 modulation by C. trachomatis in controlling inflammatory signals during infection.
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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 |
http://linkedlifedata.com/resource/pubmed/chemical/ADAM Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD95,
http://linkedlifedata.com/resource/pubmed/chemical/Extracellular Signal-Regulated MAP...,
http://linkedlifedata.com/resource/pubmed/chemical/Histocompatibility Antigens Class I,
http://linkedlifedata.com/resource/pubmed/chemical/Histocompatibility Antigens Class II,
http://linkedlifedata.com/resource/pubmed/chemical/MAP Kinase Kinase Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Tumor Necrosis Factor...,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Tumor Necrosis Factor...,
http://linkedlifedata.com/resource/pubmed/chemical/tumor necrosis factor-alpha...
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0021-9258
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
7
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pubmed:volume |
283
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
6438-48
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:18167350-ADAM Proteins,
pubmed-meshheading:18167350-Antigens, CD95,
pubmed-meshheading:18167350-Apoptosis,
pubmed-meshheading:18167350-Chlamydia Infections,
pubmed-meshheading:18167350-Chlamydia trachomatis,
pubmed-meshheading:18167350-Extracellular Signal-Regulated MAP Kinases,
pubmed-meshheading:18167350-Histocompatibility Antigens Class I,
pubmed-meshheading:18167350-Histocompatibility Antigens Class II,
pubmed-meshheading:18167350-Humans,
pubmed-meshheading:18167350-Inflammation,
pubmed-meshheading:18167350-Jurkat Cells,
pubmed-meshheading:18167350-MAP Kinase Kinase Kinases,
pubmed-meshheading:18167350-MAP Kinase Signaling System,
pubmed-meshheading:18167350-Receptors, Tumor Necrosis Factor, Type I,
pubmed-meshheading:18167350-Receptors, Tumor Necrosis Factor, Type II,
pubmed-meshheading:18167350-U937 Cells
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pubmed:year |
2008
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pubmed:articleTitle |
Reduced display of tumor necrosis factor receptor I at the host cell surface supports infection with Chlamydia trachomatis.
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pubmed:affiliation |
Research Group for Molecular Infection and Tumor Biology, Max Planck Institute for Infection Biology, Charitéplatz 1, Berlin, Germany.
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pubmed:publicationType |
Journal Article
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