Richard Cornall

FRCP, FMedSci

Nuffield Professor of Clinical Medicine and Head of Department

Professor of Immunology
MRC Investigator

Our aim is to understand how the immune system is formed and regulated and the causes of autoimmunity, particularly the systemic autoimmune diseases, and the development and selection of B cells. Adverse immunological reactions to self and foreign antigens that lead to autoimmune or inflammatory disease place a major economic and social burden on world health and individual quality of life. We are also interested in how people differ in their inherited susceptibility to these diseases and why these differences are sustained in human populations by natural selection. Advances in this area will have a large and impact on the management of human disease.

Our strategy involves research programmes in basic biology and in clinical medicine. In the first, we use transgenic models to investigate how lymphocytes function in health and in human disease and how our genes encode susceptibility to autoimmunity and immunodeficiency. In the second, which is a collaboration with Professor Simon Davis, we are developing ways to change the function of lymphocytes, turning them on in cancer and off during inflammation or autoimmunity.

Recent publications

B cells require DOCK8 to elicit and integrate T cell help when antigen is limiting

Deobagkar-Lele M. et al, (2024), Science Immunology, 9

Antibody agonists trigger immune receptor signaling through local exclusion of receptor-type protein tyrosine phosphatases

Lippert AH. et al, (2024), Immunity, 57, 256 - 270.e10

Tissue-Resident Memory T Cells in Pancreatic Ductal Adenocarcinoma Coexpress PD-1 and TIGIT and Functional Inhibition Is Reversible by Dual Antibody Blockade.

Pearce H. et al, (2023), Cancer immunology research, 11, 435 - 449

Prolidase Deficiency Causes Spontaneous T Cell Activation and Lupus-like Autoimmunity

Hodgson R. et al, (2023), The Journal of Immunology, 210, 547 - 557

NDRG1 is induced by antigen-receptor signaling but dispensable for B and T cell self-tolerance

Hodgson R. et al, (2022), Communications Biology, 5

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