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School of Biochemistry and Immunology

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About our research interests

NK cell immunometabolism:

We have recently developed a research programme in the area of NK cell immunometabolism. This work is done in collaboration with Dr. David Finlay. We were among the first to define NK cell metabolic reprogramming in NK cells, some of the regulatory mechanisms involved (mTORC1) and how metabolism can impact on NK cell function. My particular focus is on human NK cells and we have defined different metabolism profiles in CD56bright and CD56dim cell subsets. Some of this work has already been published (Journal of Immunology, 2014 & 2016) and we have recently published a manuscript describing the importance of the citrate malate shuttle in NK cells in Nature Immunology (2017). Other publications, including the integration of receptor signalling and cytokines on metabolism, and the role of TGF-b in human NK cell metabolic reprogramming (submitted to Journal of Immunology) are in the pipeline. Our work on murine NK cells aims to define the molecular mechanisms and signalling underpinning NK cell metabolic reprogramming. Projects include understanding the role of PKM2 in NK cell metabolism and the contribution of receptor signalling in the regulation of NK cell metabolism.

NK cells in chronic viral infection: HIV-1 and HCV

I have a long standing interest in understanding how NK cells function and how this is dysregulated in human chronic diseases including HIV-1 (publications in 2011 and 2013) and HCV infection (publications in 2011, 2013, 2014, 2016), and cancer (2015), and have many successful clinical collaborations that facilitate this work. We are also trying to understand how NK contribute to successful vaccination and are currently involved in a human clinical trial with novel HIV-1 and HCV vaccines (Peachi at Oxford University).

NK cell metabolism in cancer:

We have started to translate our findings on basic NK cell metabolism into particular disease states to understand how altered NK cell metabolism may contribute to chronic disease. In particular, we know that NK cell functional responses are impaired in cancer patients and we propose that this is in part due to alterations in their metabolic responses. We have already generated some data to suggest that during metastatic breast cancer, NK cell metabolism is impaired.