Although checkpoint inhibitors (CPI) have become indispensable pillars of tumor immunotherapy, responses to CPI show substantial intra- and interindividual heterogeneity. Moreover, immune-related adverse events (irAEs) represent a major challenge during or after CPI, limiting the overall benefits of immunotherapy. 

We aim to decipher the mechanisms that drive irAEs after CPI, with a particular focus on chemokines and chemokine receptors involved in the cross-talk of dendritic cells and T cells. Our goal is the identification of markers and pathways that could enable the manipulation of the immune responses in patients and might decrease the rate and severity of irAEs. For this purpose, we perform in vivo and in vitro studies, and analyse primary patient samples.