Source:http://linkedlifedata.com/resource/pubmed/id/12874014
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
14
|
| pubmed:dateCreated |
2003-7-22
|
| pubmed:abstractText |
The nonclassical HLA-G molecule exhibits a limited tissue distribution and exerts multiple immune regulatory functions. Recent studies indicate that HLA-G expression plays a key role in the induction of immune tolerance and may represent a novel immune escape mechanism of tumor cells. Despite a high frequency of tumor-infiltrating T lymphocytes in renal cell carcinoma (RCC) lesions, outgrowth of tumor cells occurs that might be attributable to abrogation-efficient antitumor responses. To delineate the potential role of HLA-G in RCC immunology, the HLA-G expression pattern and its functional consequences on immune responses were analyzed in cell lines and lesions derived from primary RCC lesions. A heterogeneous constitutive and IFN-gamma-inducible HLA-G mRNA and protein expression was found in 12.5% of RCC cell lines but not in autologous normal kidney cells. Western blot analysis of 37 primary RCC lesions revealed HLA-G protein expression in 27% of RCC lesions. Functional studies performed with alloreactive natural and lymphokine-activated killer cells as well as antigen-specific CD8(+) T-cell populations demonstrated that HLA-G expression inhibits lysis of RCC cells by these different immune effector cells, whereas HLA-G(-) normal kidney cells were recognized. Furthermore, the HLA-G-mediated counteraction of immune response could be restored by antibody blocking experiments. Thus, aberrant HLA-G expression is found at a relatively high frequency in RCC and might participate in evasion of these tumor cells from immunosurveillance.
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| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:month |
Jul
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| pubmed:issn |
0008-5472
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:day |
15
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| pubmed:volume |
63
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
4107-11
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| pubmed:dateRevised |
2011-11-17
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| pubmed:meshHeading |
pubmed-meshheading:12874014-Adult,
pubmed-meshheading:12874014-Aged,
pubmed-meshheading:12874014-Carcinoma, Renal Cell,
pubmed-meshheading:12874014-Cell Membrane,
pubmed-meshheading:12874014-Female,
pubmed-meshheading:12874014-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:12874014-HLA Antigens,
pubmed-meshheading:12874014-HLA-G Antigens,
pubmed-meshheading:12874014-Histocompatibility Antigens Class I,
pubmed-meshheading:12874014-Humans,
pubmed-meshheading:12874014-Kidney Neoplasms,
pubmed-meshheading:12874014-Killer Cells, Lymphokine-Activated,
pubmed-meshheading:12874014-Killer Cells, Natural,
pubmed-meshheading:12874014-Male,
pubmed-meshheading:12874014-Middle Aged,
pubmed-meshheading:12874014-RNA, Messenger,
pubmed-meshheading:12874014-T-Lymphocytes, Cytotoxic,
pubmed-meshheading:12874014-Tumor Cells, Cultured,
pubmed-meshheading:12874014-Up-Regulation
|
| pubmed:year |
2003
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| pubmed:articleTitle |
Functional role of human leukocyte antigen-G up-regulation in renal cell carcinoma.
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| pubmed:affiliation |
Third Department of Internal Medicine, Johannes Gutenberg University, 55101 Mainz, Germany.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|