Abstract |
Loss or downregulation of MHC class I molecules on tumour cells is a common mechanism by which tumours can escape from T-cell mediated immune responses. In this study we have investigated the immunologic crossreactivity between murine tumour cell lines expressing human papilloma virus (HPV) 16-derived E6/E7 oncoproteins with distinct surface expression of MHC class I molecules. The aims of this study were to demonstrate whether immune responses capable of coping with MHC class I-positive tumours can also be effective against their MHC class I-deficient derivatives and whether it is possible to induce immunity against MHC class I-deficient tumours by cellular vaccines based on MHC class I-deficient tumour cell lines. Our data showed that immunization with MHC class I-deficient but not with MHC class I positive tumour cells inhibited the growth of MHC class I-deficient tumours. In vivo depletion studies revealed that the mechanisms underlying effective immune responses against MHC class I-negative tumours in animals immunized with MHC class I-deficient tumour cells involved natural killer cells. The presented findings are of particular clinical relevance in the sense of construction of vaccines directed against a broad spectrum of HPV-associated tumours.
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Authors | Milan Reinis, Jana Símová, Marie Indrová, Jana Bieblová, Hana Pribylová, Simona Moravcová, Tána Jandlová, Jan Bubeník |
Journal | International journal of oncology
(Int J Oncol)
Vol. 30
Issue 4
Pg. 1011-7
(Apr 2007)
ISSN: 1019-6439 [Print] Greece |
PMID | 17332942
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Cancer Vaccines
- Histocompatibility Antigens Class I
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Topics |
- Animals
- Cancer Vaccines
(therapeutic use)
- Cell Line, Tumor
- Cell Proliferation
- Cross Reactions
- Histocompatibility Antigens Class I
(analysis, immunology)
- Human papillomavirus 16
(immunology)
- Immunization
- Mice
- Mice, Inbred C57BL
- Neoplasms
(immunology, therapy, virology)
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