The size of the peripheral T cell pool is remarkably stable. Although T cells expand massively as a result of infection, their numbers return to baseline levels after the pathogen has been eliminated.

This suggests that autoregulatory processes control the homeostasis of the peripheral T cell pool. Interleukin-7 (IL-7) plays a central role here. Although the importance of IL-7 in maintaining T-cell homeostasis is well documented, little is known about the biology of IL-7-producing cells and the mechanisms that control IL-7 production at the molecular level. In the Molecular Immunology group we address these questions using new mouse models and use them to study the immunomodulatory function of IL-7-producing stromal cells and their influence on T cell homeostasis under physiological and pathophysiological conditions.

The formation of immunological memory protects the organism from recurring infections. This special property of the immune system is used in the clinic. For example, vaccinations and adoptive T-cell therapy for malignant and viral diseases aim to generate long-lived memory T-cells (T_M).

However, the molecular mechanisms that influence T_M formation and differentiation are largely unclear. We were able to show that interferon-gamma (IFN-gamma) influences both processes both directly and indirectly. While IFN-gamma signals limit CD8⁺ T_M formation in host cells, IFN-gamma signals regulate T_M differentiation in CD8⁺ T cells. We are studying in a mouse model, via which cellular and molecular mechanisms IFN-gamma controls the formation/differentiation of CD8⁺ T_M and how these influence the elimination of pathogens as well as adoptive T cell therapy in cancer.

Contact

Prof. Dr. rer. nat. Thomas Schüler