Research at the Molecular T cell Immunology Group investigates the cross-talk of T-cell subsets with the blood coagulation system.
We previously showed that hepatic T cells contribute to atherosclerosis development in mice fed a cholesterol-containing “Western” diet. Based on these results we want to quantify specific T-cell responses against liver-derived antigens in hypercholesterolemic mice and patients with cardiovascular disease. T-cell activation will be monitored through antigen-induced expression of CD40L and FOXP3 isoforms, respectively.
T-cell differentiation in the liver depends on the micro-environment. The identification of specific conditions that alter proliferation, differentiation and migration of T cells will help to regulate T-cell-mediated disease development, such as atherosclerosis and ischemia-reperfusion injury. Our current approach targets the intracellular and extracellular levels of polyphosphate (PolyP) and the PolyP-driven intrinsic blood coagulation system using genetically altered murine models. PolyP serves as energy storage pool and mediators of the blood coagulation cascade exert inflammatory reactions. We aim to elucidate PolyP-mediated functions in T-cell subsets and to target these mechanisms via transfections of PolyP-degrading phosphatase into hepatocytes and CD4+ T cells. Our research offers the opportunity to modulate liver-specific T cell responses and provides novel strategies for cardiovascular disease treatment.
- Wissenschaftlicher Arbeitsgruppenleiter