Cold shock proteins fulfill cell-specific tasks in inflammatory diseases. In YB-1 whole body knockout animals the inflammatory response is ablated and fibrosis reduced when experimental kidney diseases are induced. With cell-specific depletion of YB-1 in monocytes/granulocytes/macrophages the inflammatory cell recruitment is enhanced. The project addresses at the molecular level, how YB-1 affects the monocytic cell phenotype, which functions extracellular YB-1 executes and how the expression of the cold shock protein is regulated in circulating immune cells in inflammatory diseases.
Collaborative Research Centre 854
Molecular organisation of cellular communication within the immune system
