The research activities realized at the Institute for Immunology concern various aspects of the induction of innate and adaptive immune responses. As part of our investigations of the innate immune system we analyze the function and regulation of mast cells and neutrophils. Of special interest are the consequences of tissue-specific interactions of these cells, for example in the skin, with members of the adaptive immune system, e.g. T cells. These studies are paralleled on one hand by research activities addressing the role of different populations of dendritic cells in the skin and in peripheral lymphoid organs where tolerance and induction of antigen-specific immunity is established. On the other hand, we are interested in the role of different cytokines in the differentiation of T cells and the function of regulatory T cells. The analysis of T cell differentiation is focused on transcriptional regulation of the development and function of different T helper cell populations, such as Th2, Th9 and Th17 cells. Furthermore, we study the function of regulatory T cells which play an essential role in maintaining the immunological tolerance in the periphery. Of special interest is the influence of this subpopulation on the activity of dendritic cells and also CD4 and CD8 positive T cells. Malfunctions of regulatory T cells are therefore associated with the development of allergic and autoaggressive diseases as well as tumors and chronic infections. For this reason, studies on the understanding of the inhibitory mechanisms of regulatory T cells including surface molecules and molecular pathways play a central role.
In addition, we perform studies leading to a better understanding of antigen processing and presentation of MHC Class I ligands in tumors and virus-infected cells as well as the induction of antigen-specific immune responses. Through local but also international cooperations, we are particularly interested in the correlation of protein expression and degradation rates and the production of MHC class I ligands.