Research
Pro-inflammatory effector T cells (Teffs) defend our bodies from infections and the growth of cancerous cells. Decreased function of Teffs is a contributing factor in the development of chronic infections and cancer whereas over-activation of their pro-inflammatory activities results in autoimmunity and/or inflammation. Teffs use effector molecules to destroy diseased cells and a critical determinant of the efficacy of Teffs is their ability to produce millions of effector molecules in response to inflammatory cues. The synthesis of effector molecules is dependent on protein synthesis -a demanding process that requires a plentiful supply of cellular energy and amino acid building blocks.
During immune responses, Teffs may be subjected to oxygen deficiency (or hypoxia). Hypoxia stimulates cells to increase the abundance of enzymes that promote oxygen-independent metabolic pathways. Therefore, when Teffs are experiencing hypoxia, in addition to producing effector molecules, it may be necessary for Teffs to generate millions of protein molecules in order to adapt and survive in oxygen-deficient environments. The need to synthesise so many proteins may put cells under substantial biosynthetic stress. My research explores how the response to hypoxia is triggered in Teffs from a translational point.
