Introduction - Apoptosis Signaling Laboratory | Department of Biochemistry and Molecular Biology

Our goal is to identify the processes by which macrophages take up dead cells, prevent inflammation and support tissue regeneration during efferocytosis. Our research group was founded in 1993. At that time, we were primarily interested in the role of transglutaminase 2 (TG2) in the cell death program, because the enzyme was often expressed where cells had died. We identified several of its functions, but in the end it turned out that the cells die well even without TG2. However, the removal of dead cells became disturbed due to the lack of TG2 in the engulfing macrophages and this led to the development of an autoimmune disease in mice. Examining the role of TG2 led us to understand the process of clearing dead cells and the central role of this process in maintaining tissue turnover, shutting down inflammation, preventing the development of autoimmune diseases, and regulating tissue regeneration. We have also shown that it regulates the differentiation of thymocytes and is also necessary for the development of skeletal muscle. After that, we also described another enzyme, retinol saturase, that it is necessary for phagocytosis in macrophages and that its absence also leads to autoimmune disease. We have shown that the appropriate amount of phagocytosis is also necessary for skeletal muscle regeneration and that muscle cells are also efficient phagocytic cells and that this ability can be regulated similarly to macrophages. Our work identified several drug attack points that can be used to influence these processes.