DISSIMILAR IMMUNOGENICITIES OF ELA AND E7 ONCOPROTEINS

National Jewish Health, Denver CO

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Abstract

The purpose of the project is to use the MCA-102 model system to elucidate the immunologic mechanisms involved in the rejection of E1A- but not E7-expressing tumor cells, genetically define the components of ElA that are required to induce robust cellular immunity, and further characterize the molecular basis by which ElA but not E7 induces a vigorous cellular immune response in two specific aims. Specific Aim 1: Elucidate the key immunologic mechanisms involved in the rejection of tumor cells expressing ElA but not E7. Specifically they will determine the interrelationship and function of NK cells, T cells, perforin- and Fas-mediated lysis and the cytokines, IL-12 and IFNg, in the rejection of E1A- but not E7-expressing tumor cells. Specific Aim 2: Define the molecular mechanisms by which E1A-p300 binding and ElA- exon 2 expression activate the NK cell response, thereby triggering a robust cellular immune response against E1A-expressing tumor cells.