Molecular T cell immunotherapy and inhibition of tumor immune escape mechanisms
We have demonstrated that (i) the tumour suppressor p53-encoded D133p53a isoform functions as a novel enhancer of cellular resilience of antitumoural TCR-engineered T cells and (ii) arginase 1 inhibition unleashes a highly potent T cell stimulatory activity within the secretome of human granulocytes. We now want to fully characterize the hyperactivated T cells, identify the molecular correlate of the hyperstimulatory activity and analyse its therapeutic potential in conjunction with D133p53a T cell modification. The tumour microenvironment will be studied in depth and our novel strategy will be extended to other tumour and infectious disease models within the CRC.
(Photos: Universitätsmedizin Mainz)