Dr Katherine Bull is an MRC-Kidney Research UK Professor David Kerr Clinician Scientist, and an Honorary Consultant Nephrologist.
Outline of REsearch
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 fateDeficiency in the metalloproteinase prolidase results in a very rare condition with recurrent infections and in some cases autoimmune features including renal immune complex disease. In vivo knock out of the PEPD gene has identified key functions for prolidase in autoimmunity, renal disease and T cell differentiation.
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
SARS-CoV-2-Specific T Cell Responses Are Not Associated with Protection against Reinfection in Hemodialysis Patients
Shankar S. et al, (2022), Journal of the American Society of Nephrology, 33, 883 - 887
Source data for:
Hodgson et al, NDRG1 is induced by antigen-receptor signaling but dispensable for B and T cell self-tolerance, Communications Biology 2022
Hodgson R. et al, (2022)