Following a PhD in cellular immunology with Peter Beverley in London, Professor Drakesmith moved to Oxford to work with Alain Townsend on the function of the HFE gene, mutants of which had recently been identified as causing hereditary haemochromatosis.
The sequence and structural similarity of the HFE protein and MHC proteins suggested there are evolutionary and molecular links between immunity and iron metabolism. This theme was reinforced by the subsequent discovery of hepcidin, a small peptide resembling anti-microbial defensins, but which is now considered to be the master hormonal regulator of iron homeostasis.
Professor Drakesmith's team is defining how hepcidin is modulated during infections, by testing which aspects of pathogen recognition by the host influence hepcidin synthesis. Their aim is to assess whether deliberately altering hepcidin can control experimental infections of iron-requiring bacterial strains.
Professor Drakesmith and colleagues have made important contributions to our understanding of the role of hepcidin in human genetic disease, in paediatric anaemia, in infection, including malarial anaemia, and in elaborating hepcidin as a diagnostic tool.