GWAS variants pose an incredible opportunity to discover new drug targets as they are the genetic anchor to the disease-causing biological processes. In my talk, I will present how my team utilises a toolkit of genomics approaches coupled with immune phenotyping at scale to link disease genes to dysregulated cell functions.
We used single-cell eQTL mapping to define gene expression regulation during CD4+ T cell activation time course. We identified that disease variants colocalised with genes dynamically regulated during T-cell activation, i.e. genes whose eQTL effects manifested at specific activation time points. We are following up on the effects of eQTL genes colocalising with disease variants using CRISPR approaches coupled with rich phenotypic cell screens and high-content imaging to enable multi-modal profiling of immune cell biology at scale.