2017: Thomas Riffelmacher
Dr Riffelmacher completed his DPhil with Prof Sten Eirik Jacobsen (NDCLS-WIMM) and Katja Simon (NDORMS). He explored the role that autophagy, a cellular recycling pathway, has during the differentiation of blood and immune cells. He was awarded the Prize for establishing a new mechanism by which autophagy controls differentiation and for his entrepreneurial spirit. Dr Riffelmacher's DPhil was funded through a WIMM Prize Studentship.
After my B.Sc in Chemistry and Biochemistry and my M.Sc in Cell Biology at LMU Munich, Germany, I was offered the unique opportunity to undertake a DPhil within the Radcliffe Department of Medicine. Continuing my path from basic Chemistry/Biochemistry towards applied and translational medical research is a logical part of my big dream to make a scientific discovery that will improve human health. I was immensely fortunate to be able to join Prof Katja Simon´s group with co-supervision by Prof Sten Eirik Jacobsen, two fantastic mentors that together made this a challenging, rewarding and also fun experience.
The main focus of my DPhil has been to explore the role that autophagy, a cellular recycling pathway, has during the differentiation of blood and immune cells. I discovered that autophagy can degrade lipid droplets in neutrophil precursors to generate the large amounts of molecular energy-currency (adenosine triphosphate) required to sustain differentiation. By breaking down lipid droplets into free fatty acids, autophagy fuels a respiration pathway in the mitochondria, the energy-producing factories of cells, to enable differentiation. Exploring the wider relevance of this pathway, I found evidence that it may also be relevant to the differentiation of other immune cells, which ultimately led to publications in Immunity, eLife, FEBS J, Autophagy and CDDis journals.
Informed by my findings, we and others found defects in the autophagy pathway associated with acute myeloid leukaemia, a disease that is characterised by immature myeloid precursors which are blocked in their differentiation. Going forward, I will attempt to exploit our new insights to target the differentiation block in myeloid leukemia during a short post-doctoral project in Oxford, before I will join Mitch Kronenberg´s group in San Diego to work on inflammatory mechanisms of NKT cells.