Dr Hamish King is a Laboratory Head at the Walter and Eliza Hall Institute (WEHI) and an internationally recognised leader in human immunology and gene regulation. He trained at the University of Oxford (Prof. Rob Klose) and Queen Mary University of London (Dr Louisa James). His work has defined mechanisms of chromatin-based control of gene expression regulation, alongside influential studies of human B cell states and immune heterogeneity using single-cell genomics. At WEHI, his research integrates functional genomics, single-cell multi-omics, and genome engineering to define how genetic variation perturbs immune cell function in human disease, with a focus on B cells and autoimmunity. He has published >30 manuscripts with >8,500 citations (h-index 23) in Cell, Nature, Science, Science Immunology, Nature Immunology, and Genome Research, including multiple first and senior author papers. He has been awarded over $5.5m in competitive funding, including a prestigious Sir Henry Wellcome Fellowship (UK) and two NHMRC Ideas Grants. He chairs the WEHI Reconciliation Committee, contributes to the scientific community through conference organisation (Oz Single Cells), is regularly invited to speak internationally (>20 invitations), serves on the editorial board of Genome Biology, and reviews for leading journals and funding bodies.
Dr King will present two recent studies from the King lab at WEHI addressing genetic and cellular mechanisms of immune dysfunction in autoimmunity and immunodeficiency. The first study resolves a major limitation of genome-wide association studies by functionally linking non-coding risk variants to gene regulation. By integrating fine-mapped variants across multiple autoimmune diseases with high-throughput single-cell CRISPR perturbation in primary human B cells, the study identifies hundreds of cis-regulatory effects across risk loci. Many variants regulate multiple genes and converge on shared transcriptional pathways, highlighting coordinated regulatory networks rather than isolated effects, including a gain-of-function variant controlling REL/cREL expression that may amplify network-wide effects through transcription factor activity. In a second study, Dr King and his team have defined the immune cell landscapes in specific antibody deficiency (SAD) and common variable immunodeficiency (CVID) used single-cell multi-omics profiling, before and after vaccination. In addition to shared phenotypes between the two cohorts, including reduced plasma cells, impaired NF-κB pathway activation, and failure to induce appropriate transcriptional responses following vaccination, they discover novel features of SAD including a previously unknow expansion of cytotoxic T cells. By analysing vaccination responses across this spectrum of health and immunodeficiency, they identify a rapid expansion of FAShigh class-switched memory B cells that correlates with the antigen-specific response to vaccination.