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.
Prof. Dr. Markus Munder & Prof. Dr. Matthias Theobald
(Photos: Universitätsmedizin Mainz)