Molecular T cell immunotherapy and inhibition of tumor immune escape mechanisms (06)

• Subject Area: Immunology
• Term: since 2018
• Project identifier: Deutsche Forschungsgemeinschaft (DFG) - Project number 318346496

We have demonstrated that (i) the tumour suppressor p53-encoded 133p53 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 33p53 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.

• DFG Programme: Collaborative Research Centres
• Subproject of: SFB 1292: Targeting convergent mechanisms of inefficient immunity in tumors and chronic infections
• Applicant Institution: Johannes Gutenberg-Universität Mainz
• Project Heads: Professor Dr. Markus Munder; Professor Dr. Matthias Theobald