Molecular mechanism of memory-like regulatory T cells in autoimmune diabetes

• Antragsteller: Professor Dr. Markus Feuerer
• Fachliche Zuordnung: Immunologie
• Förderung: Förderung von 2005 bis 2008
• Projektkennung: Deutsche Forschungsgemeinschaft (DFG) - Projektnummer 5449008

The immune system discriminates between self and nonself, establishing and maintaining unresponsiveness to self. How this is achieved has been a key issue in the field of immunology for the last decades. Naturally occurring CD4+ regulatory T cells (Tregs), the majority of which express CD25, are engaged in dominant control of self-reactive T cells, thereby contributing to the maintenance of immunologic self-tolerance. Tregs are hererogeneous in phenotype, function, and the way of generation. The aim of this project is to characterize molecular mechanisms of memory-like regulatory T cells. Recently we decribed a population of CD4+ regulatory T cells expressing the integrin ¿Eß 7. These cells share certein characteristics with memory/- effector T cells and can be found in inflammatory lesions. In a diabetes model, antigen-specific regulatory T cells coexist within the pancreatic lesion. These Tregs inhibit the final step of ß -cell destruction and rescue the mice from getting diabetes. In a genome-wide microarray analysis we found some genes to be overexpressed in these Tregs. Among these, certain prominent ones were members of two gene families encoding molecules that might interact: the annexins and S100s. We want to learn whether these molecules are essential for Treg function to suppress autoimmune diabetes. Such mouse models are very convenient for manipulating the function of Tregs and identifying important mechanisms in Treg biology.

• DFG-Verfahren: Emmy Noether-Auslandsstipendien
• Gastgeberin: Professorin Dr. Diane Mathis