King Lab

In normal and healthy cells, the activity of genes encoded in our DNA must be precisely controlled to prevent disease. My lab studies exactly how errors in this gene regulation can change the behavior and function of B cells, an important cell type in our immune system that makes antibodies to fight and remember infections.

We use advanced genomics and bioinformatics to understand how specific proteins interact with and regulate DNA in B cells, as well as examining how changes in the DNA sequence disrupt normal gene activity to cause autoimmune diseases like lupus, multiple sclerosis and rheumatoid arthritis.

Our long-term mission is to discover new treatments and diagnostic tools for patients living with autoimmune diseases through understanding the (epi)genetic pathways that drive immune dysfunction.

We aim to achieve this by moving beyond traditional approaches and applying cutting-edge single-cell and high-throughput functional genomics to patient-derived tissue and primary cells as an important advance in the field.

Our research program is making fundamental and unexpected discoveries into the genetic causes and pathogenesis of autoimmune diseases – outside of current thinking – to provide important breakthroughs in immunology research and expedite novel clinical opportunities.

Our lab has used single-cell technologies to discover novel human immune cell states and found the germinal centre-specific regulatory potential of autoimmune risk loci. These discoveries rewrite our textbook knowledge of human B cell maturation and provide new insights into the genetic aetiology of autoimmune disease.

Our datasets and methods used to make these discoveries are widely used by the research community to better understand B cell cancers, autoimmune disease, and immunodeficiency in emerging studies.

We have also made other important contributions to scientific knowledge by dissecting the fundamental mechanisms of chromatin-associated proteins in controlling how genes are turned on and off.