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Immunization with MHC class I-negative but not -positive HPV16-associated tumour cells inhibits growth of MHC class I-negative tumours.

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.
AuthorsMilan Reinis, Jana Símová, Marie Indrová, Jana Bieblová, Hana Pribylová, Simona Moravcová, Tána Jandlová, Jan Bubeník
JournalInternational journal of oncology (Int J Oncol) Vol. 30 Issue 4 Pg. 1011-7 (Apr 2007) ISSN: 1019-6439 [Print] Greece
PMID17332942 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Cancer Vaccines
  • Histocompatibility Antigens Class I
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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