Development of cancer usually occurs in later life through uncontrolled growth of mutated cells that are escaping immunosurveillance - a multi-facetted process of interactions between tissues and immune cells. Cancer rejection is for the most part ascribed to T cells, which differentiate between self and foreignness of epitopes recognized by their T cell receptor. Selective manipulation of some of these regulatory circuits led to the groundbreaking success of immune checkpoint blockade, first for the treatment of melanoma, and in the meantime for increasing numbers of other solid tumors. However, not all patients benefit from these therapies underlining the urgent need to better understand the mechanisms behind immune checkpoint blockade.
We are interested in the construction of models predicting the outcome of immune checkpoint blockade by combining clinical and immunomonitoring data, like high-dimensional in situ proteomics imaging, polychromatic, spectral and mass cytometry or single cell gene expression analyses in solid cancers. Furthermore, we aim to contribute to a better understanding of the interplay between the immune system and the tumor through intensive studies of different peripheral and tumor-invasive T cell subsets, as well as immune suppressors, with the ultimate goal of developing novel therapeutic concepts.
A major focus of our research is the investigation of role and function of γδ T cells in cancer rejection. These unconventional T cells bridge adaptive and innate immunity, have potent cytolytic functions, and do not act HLA-restricted. As a member of the DFG FOR2799 “Receiving and translating signals via the γδ T cell receptor" , our goal is to identify tumor-rejecting featuers of these unconventional T cells in order to exploit them for new immunotherapy strategies.
