Biography:
I am a postdoctoral fellow in Michael Karin laboratory at the University of California, San Diego, where I study mitochondrial stress, immunological signaling and autoimmunity. Following our recent finding that oxidized mitochondrial DNA (Ox-mtDNA) works as an inflammation alarmin, we have established a model of lupus-like disease in which circulating cell-free Ox-mtDNA leads to systemic autoimmunity. This work showing that, circulating Ox-mtDNA, rather than simply a disease biomarker of metabolic and autoimmune disorders, indeed drives autoimmune pathogenesis, has laid the foundation that I can study the Ox-mtDNA sensing subsets-plasmacytoid dendritic cells (pDCs), in autoimmunity.
My overall research goal is to define the immunological mechanisms controlling autoimmune diseases through collaboration between immunology basic researchers and clinicians. I aim to translate our work to advance human immunobiology, with safe and effective autoimmune therapies, and improve human health. Thanks so much to this ANRF award, I can continue developing my research program in autoimmunity.
Research Summary:
The proposed research is relevant to the rheumatic diseases because systemic lupus erythematosus (SLE) represents as a devastating autoimmune disease which can result in substantial morbidity and mortality. Heterogeneity in clinical manifestations and patient response to therapy delays successful clinical trials. Upon conclusion in this proposal, we will understand the intricate roles of plasmacytoid dendritic cells (pDCs) in autoimmunity, aside from the type I interferons production, and this discovery will stimulate the opening of a new avenue in autoimmune diagnosis and therapeutics directed by targeting antigen-presenting pDCs
