Department of Pathology

Professor Chris Rudd

Research description

Our laboratory is interested in the field of signal transduction, immunity and immune pathologies.  Our major interest concerns the identity and function of receptors/co-receptors and signalling pathways in T-cells and the way in which alterations in these pathways lead to disease states such as autoimmunity.

We were the first to discover that cell surface receptors can interact with protein kinases with the identification of the CD4- and CD8- p56lck complexes. Protein kinases transfer phosphate groups to target proteins and in the process modify the function of the protein. CD4- and CD8- p56lck are now accepted as the initiators of the activation cascade in T-cells. The discovery also provided a long-sought function for members of the src family (exemplified by the oncogene pp60src) in the function of normal cells. 

In recent years, we have focused on the identification of adaptor proteins or molecular scaffolds that integrate the signals sent from the surface of cells, and the nature of signalling mediated by co-receptors such as CD28 and CTLA-4.

Specific Projects:

  • Identification of novel molecular scaffolds in T-cells. Studies on the role of adaptors ADAP and SKAP-55 in regulating integrin (i.e. LFA-1) adhesion, conjugate formation and other immune cell functions (Immunology)
  • Imaging signal transduction in T-cells. Studies on the real-time imaging of signaling proteins in T-cells and their link to activation and migration (Immunology/Cellular Molecular Pathology)
  • Biochemistry of the molecular modules Studies on the role of novel SH3 domains and other modules in disease pathologies (Cellular Molecular Pathology)
  • Sumoylation in T-cell function. Studies on the sumoylation of the adaptor SLP-76 and its role in regulating microcluster formation at the immunological synpase (Immunology).
  • CD28 and CTLA-4 co-stimulation: Studies on the mechanisms of co- receptor CD28, ICOS and CTLA-4 regulation of T-cell function.  These projects involve co-receptor signalling as well as our model of reverse stop- signalling for CTLA-4 regulation of T-cell responses to antigen and autoimmune pathologies (Immunology).