Source:http://linkedlifedata.com/resource/pubmed/id/18352913
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
2008-3-20
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pubmed:abstractText |
It is known that the number of ImC, expressing myeloid markers, CD11b and Gr-1, increase with tumor growth and ImC play a role in the escape of tumor cells from immunosurveillance in tumor-bearing mice and cancer patients. However, the mechanisms by which ImC suppress immune responses in tumor-bearing mice have not been completely elucidated. In the present study, we investigated the function of splenic ImC freshly isolated from tumor-bearing mice and splenic ImC differentiated in vitro by GM-CSF. Freshly isolated splenic ImC were divided into two groups depending on Gr-1 expression, Gr-1 high (Gr-1hi) and intermediate (Gr-1int). Freshly isolated splenic Gr-1int ImC, but not Gr-1hi ImC, from tumor-bearing mice reduced production of IFN-gamma in CD8+ T cells, but neither splenic Gr-1int ImC nor Gr-1hi ImC isolated from naive mice did. Both Gr-1int and Gr-1hi ImC differentiated in vitro by GM-CSF inhibited production of IFN-gamma in both CD8+ and CD4+ T cells. In addition, the differentiated Gr-1int ImC, one-third of which were CD11c+F4/80+ cells, and their culture supernatants suppressed proliferative responses of T cells stimulated by CD3 ligation, but the differentiated Gr-1hi ImC and their culture supernatants did not. These results suggest that Gr-1int ImC are altered to immune-suppressive cells in tumor circumstances and that they are differentiated by GM-CSF progressively into CD11c+F4/80+ cells with further suppressive activity against T cells.
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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 |
Jan
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pubmed:issn |
0385-5600
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
52
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
47-53
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:18352913-Animals,
pubmed-meshheading:18352913-Antigens, CD11b,
pubmed-meshheading:18352913-CD4-Positive T-Lymphocytes,
pubmed-meshheading:18352913-CD8-Positive T-Lymphocytes,
pubmed-meshheading:18352913-Cell Proliferation,
pubmed-meshheading:18352913-Female,
pubmed-meshheading:18352913-Flow Cytometry,
pubmed-meshheading:18352913-Interferon-gamma,
pubmed-meshheading:18352913-Lymphocyte Activation,
pubmed-meshheading:18352913-Mice,
pubmed-meshheading:18352913-Mice, Inbred BALB C,
pubmed-meshheading:18352913-Mice, Inbred C57BL,
pubmed-meshheading:18352913-Myeloid Cells,
pubmed-meshheading:18352913-Neoplasms,
pubmed-meshheading:18352913-Receptors, Chemokine
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pubmed:year |
2008
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pubmed:articleTitle |
Analysis of splenic Gr-1int immature myeloid cells in tumor-bearing mice.
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pubmed:affiliation |
Department of Pathology, Shiga University of Medical Science, Ohtsu, Japan.
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pubmed:publicationType |
Journal Article
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