Autoimmune diseases, including Systemic Lupus Erythematosus (SLE), Rheumatoid Arthritis (RA), and Multiple Sclerosis (MS), affect millions worldwide, yet their etiologies remain incompletely understood. Emerging evidence suggests genetic predisposition, environmental exposures, and viral triggers that initiate or exacerbate autoimmunity. However, the complex interplay among these factors has not been fully elucidated.
This project aims to explore three key dimensions of autoimmune disease development: (1) the association between viral infections (e.g., Epstein-Barr virus, SARS-CoV-2) and autoimmune onset or progression; (2) identification of protein, metabolic, and genetic biomarkers that characterize disease subtypes and progression; and (3) the contribution of environmental exposures, such as pollutants, heavy metals, and occupational agents to autoimmune risk.
Using UK Biobank’s extensive cohort data and multi-omics resources, we will investigate the shared and unique pathways linking infections, environmental factors, and molecular dysregulation across major autoimmune conditions. Objectives include identifying viral exposure histories correlated with autoimmune diagnoses; discovering immune-related genetic variants and epigenetic changes; and defining molecular signatures in blood proteomics and metabolomics that distinguish disease phenotypes.
By integrating these factors, we aim to construct a systems-level understanding of autoimmune disease mechanisms, facilitating earlier diagnosis, improved risk prediction, and the discovery of novel therapeutic targets.
