Immune-cell metabolism is critical to function, with activation and environmental factors determining whether cells obtain sufficient substrates to meet their metabolic demands. The first part of this presentation examines how lipid composition differs across major immune-cell classes and subsets. We show that this diversity influences susceptibility to ferroptosis: lymphoid cells are susceptible, whereas myeloid cells are largely resistant. The second part explores the interplay between metabolic disorders and clonal haematopoiesis, a risk factor for cardiovascular disease. Metabolic disorders inhibit AMPK activity in haematopoietic stem and progenitor cells, promoting myeloid differentiation. In DNMT3A-mutant HSCs, AMPK activation restrains clonal expansion in mice.

About the speaker: Professor Andrew Murphy is the Head of the Heart Attack Program at the Baker Heart and Diabetes Institute. He is currently a NHMRC Investigator grant recipient. His work largely focuses on how inflammatory diseases contribute to cardiovascular disease through alterations in haematopoiesis. He has over 185 publications with >16K citations and a H-index of 67 in leading journals including Nature Medicine, Nature Cell Biology, Cell Stem Cell, Cell Metabolism, Circulation, etc.

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