Joanna Davies is a biomedical research scientist in the field of immune regulation and immune homeostasis in murine and human organ transplantation, autoimmunity, and cancer. She received her Ph.D. from the Nuffield Department of Surgery, University of Oxford, UK in Transplantation Immunology. This was followed by postdoctoral fellowships in graft versus host disease at the Medical Biology Institute in La Jolla, and in transplantation tolerance at the University of Cambridge, UK. This training in classical cellular immunology has provided an excellent foundation to address mechanisms of immune regulation in immune-mediated diseases.
Most recently, Dr. Davies has focused her research on identifying immune pathways that predict and cause disease progression in type 1 diabetes (T1D) and cancer. The clinical significance of this work is that cellular and molecular markers within these pathways might be used as targets for new therapies and to stratify patients for therapy. Using human blood samples from adult patients with either cancer or T1D, her research group has successfully identified several candidate cell subsets that might be modified therapeutically to prevent disease progression: In patients newly diagnosed with T1D, the Davies research group has identified a new population of immune cells that are almost absent from people with severe disease (1-3). These cells, now called 127-hi cells, are highly active memory T cells with a bias towards the anti-inflammatory Th2-type phenotype (4). In a multi-site study headed by Dr. Davies, with collaborators from the United States, Australia and Italy, the association between 127-hi cells and disease progression in T1D has been validated, as has their anti-inflammatory Th2 bias. Moreover, the relative frequency of 127-hi cells in T1D patients at diagnosis has the capacity to predict response to therapy in the TIDAL clinical trial (5). Current research is focused on understanding whether these cells play an active role in protecting people from T1D and whether they can be enhanced to prevent and reverse T1D.
In a separate program, the Davies group is working towards understanding why people who have been diagnosed with cancer are less likely to have a recurrence if they regularly exercise. The hypothesis being tested in that exercise enhances the function of immune cells that kill cancer cells. To this end, blood from patients with gastrointestinal cancer was screened for immune T cell changes that correlate with reduced muscle mass, and changes in muscle strength. This study has identified several T cell subsets that are associated with muscle strength and mass in patients with cancer that are not present in healthy people. These data are published in Journal of Cachexia, Sarcopenia and Muscle (6) and are the basis for a clinical trial now underway at SDBRI to test the hypothesis that exercise to increase muscle strength and mass in breast cancer survivors modifies the immune system, making it more responsive to cancer cells.
In 2013 Dr. Davies founded San Diego Biomedical Research Institute where she is currently President & CEO. Dr. Davies contributes to the scientific community through participation and membership on grant review committees for the National Institute of Diabetes and Kidney Diseases, the National Cancer Institute, and the American Diabetes Association, and by acting as reviewer for several scientific journals.
Ph.D. in Transplantation Immunology, University of Oxford, U.K.
B.Sc. (Hons) in Cellular Pathology, University of Bristol, U.K.
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