Folia Biologica
Journal of Cellular and Molecular Biology, Charles University 

It has been demonstrated repeatedly that a high proportion of tumours derived from MHC class I⁺ precursors are MHC class I^-. Since a major task in immunotherapy strategies for treatment of malignancies is to develop polyvalent tumour vaccines efficient against a broad spectrum of tumours, we have examined whether MHC class I⁺ cell-based tumour vaccines can cross-protect against homologous MHC class I^- tumour challenge and vice versa. For these purposes, we have used two oncogenic cell lines induced independently by co-transfection of murine H-2^b cells with E6/E7 HPV16 and activated Ha-ras oncogenes, the tumours TC-1 (MHC class I⁺, HPV16 E7⁺) and MK16/1/IIIABC (MHC class I^-, HPV16 E7⁺). Surprisingly, it was found that these two tumours do not cross-react, although both of them contain the crucial HPV16-coded tumour rejection antigen E7. Preimmunization with the MHC class I⁺ tumour did not protect against a subsequent challenge with the MHC class I^- tumour and vice versa; however, immunization with the TC-1 tumour could protect syngeneic mice against the TC-1 tumour challenge and, similarly, immunization with the MK16/1/IIIABC tumour could protect mice against the MK16/1/IIIABC tumour challenge. If this finding can also be confirmed as a more general phenomenon with other MHC class I⁺ and class I^- tumours, it could have serious implications for design of immunotherapeutic vaccines and protocols.

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