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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1
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pubmed:dateCreated |
2006-11-23
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pubmed:abstractText |
CD4(+)CD25(+) regulatory T cells have been characterized as a critical population of immunosuppressive cells. They play a crucial role in cancer progression by inhibiting the effector function of CD4(+) or CD8(+) T lymphocytes. However, whether regulatory T lymphocytes that expand during tumor progression can modulate dendritic cell function is unclear. To address this issue, we have evaluated the inhibitory potential of CD4(+)CD25(+) regulatory T cells from mice bearing a BCR-ABL(+) leukemia on bone marrow-derived dendritic cells. We present data demonstrating that CD4(+)CD25(+)FoxP3(+) regulatory T cells from tumor-bearing animals impede dendritic cell function by down-regulating the activation of the transcription factor NF-kappaB. The expression of the co-stimulatory molecules CD80, CD86 and CD40, the production of TNF-alpha, IL-12, and CCL5/RANTES by the suppressed DC is strongly down-regulated. The suppression mechanism requires TGF-beta and IL-10 and is associated with induction of the Smad signaling pathway and activation of the STAT3 transcription factor.
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pubmed:grant |
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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/Antigens, CD4,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD80,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD86,
http://linkedlifedata.com/resource/pubmed/chemical/Forkhead Transcription Factors,
http://linkedlifedata.com/resource/pubmed/chemical/Foxp3 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Fusion Proteins, bcr-abl,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-10,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-2 Receptor alpha Subunit,
http://linkedlifedata.com/resource/pubmed/chemical/NF-kappa B,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Transforming Growth...,
http://linkedlifedata.com/resource/pubmed/chemical/STAT3 Transcription Factor,
http://linkedlifedata.com/resource/pubmed/chemical/STAT3 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factor beta
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0340-7004
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
56
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
48-59
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pubmed:dateRevised |
2007-12-3
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pubmed:meshHeading |
pubmed-meshheading:16612596-Animals,
pubmed-meshheading:16612596-Antigens, CD4,
pubmed-meshheading:16612596-Antigens, CD80,
pubmed-meshheading:16612596-Antigens, CD86,
pubmed-meshheading:16612596-Bone Marrow Cells,
pubmed-meshheading:16612596-Dendritic Cells,
pubmed-meshheading:16612596-Female,
pubmed-meshheading:16612596-Flow Cytometry,
pubmed-meshheading:16612596-Forkhead Transcription Factors,
pubmed-meshheading:16612596-Fusion Proteins, bcr-abl,
pubmed-meshheading:16612596-Immunosuppression,
pubmed-meshheading:16612596-Interleukin-10,
pubmed-meshheading:16612596-Interleukin-2 Receptor alpha Subunit,
pubmed-meshheading:16612596-Leukemia,
pubmed-meshheading:16612596-Lymphocyte Activation,
pubmed-meshheading:16612596-Lymphocytes, Tumor-Infiltrating,
pubmed-meshheading:16612596-Mice,
pubmed-meshheading:16612596-Mice, Inbred BALB C,
pubmed-meshheading:16612596-Mice, Inbred C57BL,
pubmed-meshheading:16612596-Mice, Transgenic,
pubmed-meshheading:16612596-NF-kappa B,
pubmed-meshheading:16612596-Phosphorylation,
pubmed-meshheading:16612596-Receptors, Transforming Growth Factor beta,
pubmed-meshheading:16612596-STAT3 Transcription Factor,
pubmed-meshheading:16612596-Signal Transduction,
pubmed-meshheading:16612596-T-Lymphocytes, Regulatory,
pubmed-meshheading:16612596-Transforming Growth Factor beta
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pubmed:year |
2007
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pubmed:articleTitle |
Tumor-derived CD4(+)CD25(+) regulatory T cell suppression of dendritic cell function involves TGF-beta and IL-10.
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pubmed:affiliation |
Department of Pediatrics, Steele Children's Research Center, University of Arizona, Tucson, AZ 85724-5073, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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