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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2005-4-14
pubmed:abstractText
Low antigenicity or development of tolerance is believed to be a major contributor to the escape of malignant tumors from immune surveillance of the host. However, anti-tumor responses can be elicited by concomitant immunization of poorly antigenic tumor cells with homologous xenogeneic proteins as 'altered self' proteins. In our study, anti-tumor, but not anti-xenogeneic antigen, immune responses were generated after transduction of the gene coding for a G-protein coupled human formyl peptide receptor like-1 (FPRL1) into a mouse C26 colon cancer cell line. C26 cells transfected with FPRL1 gene exhibited markedly reduced tumorigenicity in syngeneic mice, in association with the appearance of high levels of antibody activity reacting with both FPRL1 containing and wild type C26 cells. The anti-tumor responses required the participation of CD4+ T lymphocytes, since no tumor rejection was observed in nude mice or in syngeneic mice depleted of CD4+ T cells. Furthermore, mice primed with FPRL1 transfected C26 cells were resistant to subsequent challenge by wild type C26 cells. These results indicate that the presence of human FPRL1 is capable of triggering specific anti-tumor host immune responses against poorly antigenic mouse tumor cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1567-5769
pubmed:author
pubmed:issnType
Print
pubmed:volume
5
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
971-80
pubmed:dateRevised
2008-5-6
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
Transduction of the gene coding for a human G-protein coupled receptor FPRL1 in mouse tumor cells increases host anti-tumor immunity.
pubmed:affiliation
Laboratory of Tumor Immunobiology, Cancer Research Institute, Xiang-Ya School of Medicine, Central South University, PR China. jinyueh@yahoo.com
pubmed:publicationType
Journal Article