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The prevalence of allergies including allergic asthma is increasing in western civilizations and there is an unmet clinical need of novel treatment strategies. It has recently been shown that asthmatic lung inflammation is especially mediated by Th17 cells in therapy-resistant patients. The aim of this project is to investigate how the energy metabolism regulates the epigenome and gene expression, and, thereby, the T cell effector function of Th2 and Th17 cells during asthmatic airway inflammation.

One promising approach in the fight against cancer is to activate the immune system to detect and fight tumor cells. However, cancer cells have evolved many ways of protecting themselves from the immune system: For example, they hide within the tumor stroma or surround themselves with a cloud of inhibitory signals that inhibits the activity of infiltrating immune cells. In this project, we want to uncover the complex relationship between changes in the tumor stroma and the presentation of antigens on the surface of tumor cells in models of colorectal cancer.

Dendritic cell vaccination (DCV) induces an anti-tumor immune response in gliobastoma patients, but efficacy seems limited. Effector T cells expressing IFNγ and T-bet can be detected in the brains of vaccinated patients, suggesting successful stimulation of tumor-specific type 1 T cells. However, these cells simultaneously express high levels of Eomes, leading to upregulation of the immune checkpoint receptor PD-1, associated with T-cell dysfunction. Thus, there appears to be a rational to combine DCV with immune checkpoint blockade (ICB) to increase therapeutic efficacy.

Preclinical studies show, that antibiotics disturbing gut bacteria reduce the effectiveness of immune therapies for cancers outside the gut (e. g. lung cancer or breast cancer). This is because antibiotics disturb the integrin signalling of immune cells in the intestine. As a result, overall trafficking of immune cells in the organism is disturbed and heavily influences immune responses in tumors distant to the intestine.

In stroke, the blockage of blood vessels leads to the death of nerve cells. The longer the blockage, the more severe the consequences. The vessels of many patients can be reopened by using blood thinners (lysis) and catheter procedures. However, reopening does not guarantee that patients will benefit. Parallel inflammatory processes lead to ongoing stroke growth. These processes have not been therapeutically addressed so far. A protein complex called the inflammasome is a major regulator in these inflammatory processes.