Project: Inflammation imaging
Accurate and specific imaging markers for activated T-cells would greatly assist in our understanding of inflammatory processes, both in Immuno-oncology (I-O) and in cardiovascular / metabolic disease.
I-O utilizes the endogenous immune response to combat tumors. In order to grow, a tumor must evade the immune system, which can be accomplished by different mechanisms, for example by suppressing activated killer T-cells. In recent years several antibody-based therapies has been developed which inhibits the suppressing ligands presented by tumors (for example PD-L1 inhibition).
The standard imaging based RECIST criteria as well as 18F-FDG measurement of tumor activity is routinely employed in anti-cancer therapy efficacy studies. However, I-O therapy has been shown to generate “pseudoprogression“ for these endpoints. Tumors ”flare” in both size and 18F-FDG avidity due to (the intended) increase in immune response and tumor infiltration by immune cells. Thus there exist an unmet clincial need of a more specific marker of the therapy mediated immune response in order to establish proof-of-mechanism and enable stratification of candidate drugs.
Our solution is to generate affibodies for surface markers specifically expressed by activated cytotoxic T-cells. We have, in collaboration with researchers at KTH identified an affibody for CD69. We expect this highly novel approach to provide a mechanistic endpoint for a tumor specific immune response – providing personalized, whole body, biopsy-free proof-of-mechanism of I-O therapies for the first time.