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- Dustin, M Group | Immunological synapse Research Group
Role of co-stimulatory/Inhibitory receptors in T cell activation and pathology
I developed a deep interest in Immunology during my undergraduate degree in Biochemistry (Imperial College London). Having completed an MSc in Integrated Immunology (University of Oxford) with a focus on intestinal immune homeostasis, I was determined to obtain a PhD in a competitive and enthusiastic scientific environment. I was granted a Kennedy Trust-funded scholarship to start a DPhil at the Kennedy Institute of Rheumatology in Prof. Michael Dustin's Lab. The Welcome Trust also funds the research through a PRF to Prof Dustin.
I started off my PhD research with an interest in elucidating the mechanisms driving aberrant chronic inflammatory immune responses, in autoimmune diseases. I investigated the role of inhibitory Natural Killer cell receptors expressed on T lymphocytes during an immune response. In particular, I looked at the KIR3DL family of receptors and how these might affect activation, proliferation and cytokine expression of T lymphocytes in the context of autoimmune arthritis like Ankylosing Spondylitis. A key tool of my research has been high and super resolution imaging techniques (TIRFM and STORM) in an effort to reveal the molecular mechanisms that could explain some of the observed effects of these receptors on T cell activation and cytokine expression. Revealing such molecular mechanisms could help understand steps in the pathogenesis of chronic inflammation and potential targets of intervention.
In parallel, I have also developed an interest in classical T cell classical co-stimulatory/inhibitory receptors whose interactions in the immunological synapse have not been fully appreciated before. Our imaging studies reveal novel localisation dynamics that can regulate signal integration during the formation of the immune synapse and hence T cell activation/differentiation. We find that such receptors might be differentially regulated in the context of certain diseases thus underlining potential pathogenic or compromised mechanisms that can explain immunopathology.