Katherine Bull

The development of new therapies for kidney disease is hampered by limited understanding of the underlying mechanistic pathways at the cellular level. This contrasts with the situation in cancer biology for example, where detailed understanding of cell biology, including the immune response, is transforming treatment. To make such advances for patients with renal disease, our objective has been to develop a variety of clinical models and tools, and then establish new approaches to interrogate tissue cellular pathology. We apply gene editing, single cell transcriptomics, and renal and immune phenotyping, to models and human samples. 

In particular our work focuses on glomerular protein leak, a hallmark of many renal pathologies. 

Examples of our work

The effects of Immune complex deposition on glomerular renal cells in lupus nephritis

Autoimmune renal disease such as occurs in Systemic Lupus Erythematosus (SLE) is characterised by the deposition of immune complexes in the renal glomeruli, but little is understood about the cellular responses in the tissue that ultimately lead to renal failure for some patients with SLE. Using inducible models and spatial transcriptomics we are interrogating cellular signals and cross talk in the kidney. 

The role of Prolidase in autoimmunity and T cell fate

Collaborators 

Richard Cornall, University of Oxford

John Todd / Diabetes and Inflammation Laboratory, University of Oxford 

Moin Saleem, University of Bristol 

Rutger Ploeg / Oxford Transplant Biobank, University of Oxford 

Beijing Genomics Institute