The King has approved that Professor Menna Clatworthy, FRCP, PhD,
FMedSci, Professor of Translational Immunology at the University
of Cambridge, be appointed to the Regius Professorship of
Medicine at the University of Oxford in succession to Professor
Sir .
Professor Menna Clatworthy
Professor Clatworthy is Professor of Translational Immunology at
the University of Cambridge, former NIHR Research Professor and
Honorary Consultant Nephrologist at Cambridge University
Hospitals NHS Foundation Trust. She is also Director of the
Cambridge Institute of Therapeutic Immunology and Infectious
Disease (CITIID), Associate Faculty in Cellular Genetics at the
Wellcome Sanger Institute, and a Fellow and previous Director of
Studies in Clinical Medicine at Pembroke College, Cambridge. Her
clinical and academic career has focused on immunology and
nephrology, with research spanning fundamental immunology,
experimental medicine and clinical research. She was elected a
Fellow of the Academy of Medical Sciences in 2020 and a Fellow of
the Learned Society of Wales in the same year, and was elected to
EMBO in 2022.
She is known for her influential work in tissue and humoral
immunity, particularly on how tissue environments shape
immune-cell function and how B-cell activation and antibody
responses are regulated in organs including the kidney and gut.
Her work has identified an unanticipated link between immunity in
the gut and the central nervous system (CNS), with direct
trafficking of gut-primed B and T cells to the meninges and
brain, changing the established dogma on how peripheral immune
stimuli in the gastrointestinal tract may influence the CNS. Her
research combines in vitro and in vivo models
with analysis of primary human tissues with single-cell and
spatial genomic and transcriptomic technologies, and has
contributed to understanding of immune responses in kidney
disease, transplantation and infection. This includes the
discovery of how the kidney microenvironment creates distinct
zones of immune defence and the identification of therapeutically
tractable, cell type-and tissue-specific targets in
autoantibody-mediated diseases.