Immune evasion within the tumour microenvironment
I am interested in immunosuppressive mechanisms within the tumour microenvironment. Cells of the immune system require signals that convey ‘danger’ and a necessity to respond. In the absence of any invading pathogen, within the tumour microenvironment ‘danger’ is signalled by the presence of cell-free nucleic acids released upon cell death. Absence of recognition of this danger leads to a less efficient adaptive immune response required to kill tumour cells. I am studying mechanisms by which cancer cells influence the recognition of nucleic acids.
I am also interested in understanding the cross-talk between stromal cells and immune cells within the tumour. Stromal cells play an integral part not only in the progression of the tumour but also in the tumour-specific immune response. Using primary human renal cell carcinoma samples, I study cancer-associated fibroblasts and the ways in which they influence the presence and function of immune cells within the tumour.
Before my work here at the MRC Human Immunology Unit, as a post-doc at the Institut Curie in Paris, I used biochemical and imaging techniques to study the molecular regulation of two receptors: PD-L1 that is a target for checkpoint inhibitor therapy in tumours; and TLR3, a nucleic acid sensor. During this time, I became interested in the regulation of nucleic acid sensing and the translational aspects of my work which brought me to Prof. Vincenzo Cerundolo’s lab at Oxford. During my PhD, using mouse models of autoimmune inflammation, I studied the peripheral generation and function of CD8+ T cells restricted to the non-classical MHC-I molecule, Qa-1.