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rdf:type |
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lifeskim:mentions |
umls-concept:C0011306,
umls-concept:C0020964,
umls-concept:C0027651,
umls-concept:C0085358,
umls-concept:C0549178,
umls-concept:C0591833,
umls-concept:C1292733,
umls-concept:C1332717,
umls-concept:C1413244,
umls-concept:C1515877,
umls-concept:C1522721,
umls-concept:C1552861,
umls-concept:C1704410,
umls-concept:C1706438,
umls-concept:C1879547,
umls-concept:C2698600
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pubmed:issue |
15
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pubmed:dateCreated |
2009-7-31
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pubmed:abstractText |
We reported previously that tumor-specific CD8(+) T cells (TcR-I) become tolerant in the transgenic adenocarcinoma of the mouse prostate (TRAMP) model. In this study, we show that CD4(+) TcR transgenic (TcR-II) T cells transferred into TRAMP mice became activated in lymph nodes, trafficked to the prostate, and initially functioned as T(H)1 cells. Although a single cotransfer of TcR-II cells delayed TcR-I cell tolerization, repeated transfer of TcR-II cells was required to prevent TcR-I cell tolerization and significantly slowed progression of TRAMP prostate tumors. After transfer of TcR-II cells, dendritic cells within the tumor expressed higher levels of costimulatory molecules and displayed an enhanced ability to stimulate proliferation of naive T cells. Blockade of CD40-CD40L interactions during TcR-II transfer resulted in a profound reduction in dendritic cell stimulatory capacity and a partial loss of TcR-I effector functions and tumor immunity. These data show that sustained provision of activated tumor-specific CD4(+) T cells alters the immunosuppressive tumor microenvironment, ultimately leading to the control of tumor growth. These findings will assist in the design of more effective immunotherapeutic approaches for cancer.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/19622771-10501846,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19622771-10786685,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19622771-10974075,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19622771-11086036,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19622771-11104805,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19622771-12594515,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19622771-12690179,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19622771-12690201,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19622771-15300249,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19622771-1532662,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19622771-15728465,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19622771-15931392,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19622771-15980149,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19622771-16622476,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19622771-17237372,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19622771-17274112,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19622771-7507387,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19622771-7724580,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19622771-7796292,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19622771-8156501,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19622771-8314354,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19622771-8439951,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19622771-8530876,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19622771-8760829,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19622771-8816378,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19622771-8837607,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19622771-9448305,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19622771-9500606,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19622771-9624004,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19622771-9624005
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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 |
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
1538-7445
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:day |
1
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pubmed:volume |
69
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
6256-64
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pubmed:dateRevised |
2010-9-24
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pubmed:meshHeading |
pubmed-meshheading:19622771-Adenocarcinoma,
pubmed-meshheading:19622771-Amino Acid Sequence,
pubmed-meshheading:19622771-Animals,
pubmed-meshheading:19622771-Antigen-Presenting Cells,
pubmed-meshheading:19622771-Antigens, CD40,
pubmed-meshheading:19622771-CD4-Positive T-Lymphocytes,
pubmed-meshheading:19622771-CD40 Ligand,
pubmed-meshheading:19622771-CD8-Positive T-Lymphocytes,
pubmed-meshheading:19622771-Dendritic Cells,
pubmed-meshheading:19622771-Immune Tolerance,
pubmed-meshheading:19622771-Immunotherapy, Adoptive,
pubmed-meshheading:19622771-Lymph Nodes,
pubmed-meshheading:19622771-Male,
pubmed-meshheading:19622771-Mice,
pubmed-meshheading:19622771-Mice, Inbred C3H,
pubmed-meshheading:19622771-Mice, Inbred C57BL,
pubmed-meshheading:19622771-Mice, Transgenic,
pubmed-meshheading:19622771-Molecular Sequence Data,
pubmed-meshheading:19622771-Prostatic Neoplasms
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pubmed:year |
2009
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pubmed:articleTitle |
Immunity to murine prostatic tumors: continuous provision of T-cell help prevents CD8 T-cell tolerance and activates tumor-infiltrating dendritic cells.
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pubmed:affiliation |
Tumor Immunity and Tolerance Section, Laboratory of Molecular Immunoregulation, Cancer and Inflammation Program, SAIC-Frederick, Inc, Frederick, Maryland, USA.
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