During my Post doc position at the Medical University Innsbruck, in the group of Gottfried Baier, I could depict how T cell receptor thresholds are regulated by the orphan nuclear receptor NR2F6. Using mouse models that mimic human multiple sclerosis I identified the molecular mechanism how NR2F6 potently antagonizes the ability of T helper 17 (Th17) CD4+ T cells to induce the expression of inflammatory cytokines and therefore suppresses autoimmunity. In the following years we characterized NR2F6 as an intracellular immune checkpoint, directly repressing transcription of cytokine genes in T cells relevant for cancer cell rejection and therefore enhancing tumor immune surveillance. We use mouse genetic deletion as well as transgenic overexpressing lines in combination with biochemical, imaging and flow cytometry during T cell dependent immune responses.

Molecular mechanisms that coordinate immune cell function under the control of nuclear receptors, especially members of the COUP-TF family; focus on immune responses during infection, autoimmune reactions and cancer immune surveillance.