Activation and termination of immune responses are balanced through cross-talk between tyrosine kinases and phosphatases immediately downstream of the T cell receptor. Changes in expression and point mutations in these molecules, in particular the cytoplasmic phosphatase PTPN22, have been linked to autoimmunity. We have been asking how these mutations perturb homeostasis and result in a failure of regulation, and at what point do perturbations in the homeostatic balance of the immune system tip into immunopathology and autoimmunity. On the flip side, can we use these mutations to improve responses of T cells, particularly in the context of immunotherapy to cancer?
Rose Zamoyska has been Professor of Immune Cell Biology at the University of Edinburgh since 2007. She obtained her PhD from the University of Cambridge and undertook postdoctoral training in Stanford, USA before moving to London where she established her research group first at University College and then as a tenured scientist at the National Institute for Medical Research in Mill Hill. The primary interest of the lab is in T cell signalling and how signals through the T cell receptor influence T cell homeostasis and the ability of T cells to be activated by antigens.