We focus on understanding how stress signals emerging from the endoplasmic reticulum (ER) sculpt the function of immune cells in health and disease. Our group uncovered that tumors provoke ER stress in infiltrating dendritic cells and T cells as a mechanism to evade immune control and promote malignant progression (Cell 2015; Cell 2017; Nature 2018). We then identified that ER stress responses in leukocytes can drive prostaglandin biosynthesis and promote pain under inflammatory settings (Science 2019). Based on these findings, our lab aims at mechanistically defining how activation of ER stress sensors under diverse pathological conditions regulate specific metabolic and epigenetic programs in immune cells. We also have a particular interest in developing new cancer immunotherapies based on disabling aberrant ER stress responses in the tumor microenvironment.
