Role of the aryl hydrocarbon receptor in immunosurveillant functions of murine dendritic epidermal T cells

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The skin is a barrier to the environment and contains immune cells, which contribute to fighting infections, wound repair or elimination of cancer cells. In this project, we focus on a particular type of immune cells, the so-called dendritic epidermal T cells (DETC). In previous work we found that a ligand-activated transcription factor, the aryl hydrocarbon receptor (AHR) controls DETC´s expression of inflammation-related genes. We now want to study, whether and how this affects the functions of DETC, such as wound repair, recognition of stressed keratinocytes, or DETC´s support against UV-damage. Mechanistically, we will study whether AHR signaling is involved in DETC metabolic changes upon activation, i.e. whether the activation-induced energy needs result in shifts from preferential oxidative phosphorylation to glycolysis. Further, we will analyze the involvement of the surface receptor CD69, a T cell activation marker, but also a molecule inflammation dampening potential, and target of AHR-signaling.