The cellular lipidome is comprised of thousands of individual lipid species each belonging to a number of structurally distinct lipid classes. Lipids influence numerous aspects of cellular physiology, with differences in lipid composition between cell types contributing to cell-specific functionality. Our laboratory has recently characterised the cellular lipidome of the human and mouse immune systems. One of the most striking effects we observed was a marked variance in the levels of polyunsaturated fatty acid (PUFA)-containing phospholipids (PL) between different immunes cell types. This was particularly intriguing as these lipid species have recently been identified as the key executioners of ferroptosis, a newly discovered form of cell death. Accordingly, we hypothesised that the distinct PUFA-PL composition of different immune cell types would dictate susceptibility to ferroptosis. Therefore, we treated immune cells isolated from murine bone marrow with ML210, an inhibitor of GPX4, the major ferroptosis suppressing pathway. Cell viability analysis revealed that T and B cells, cells with the highest abundance of pro-ferroptotic PUFA-PLs, were the most susceptible to ferroptosis. Importantly, ML210-induced cell death in T and B cells was prevented by treatment with inhibitors of ferroptosis. In contrast, neutrophils and monocytes, cells with the lowest abundance of pro-ferroptotic PUFA-PLs, were resistant to ferroptosis. Excitingly, supplementation with oleic acid and PE(18:0/18:1) respectively re-modelled the cellular lipidome of T cells, protecting them from ferroptotic cell death. Meanwhile, neutrophils supplemented with arachidonic and docosahexaenoic acids demonstrated increased sensitivity towards ferroptosis. Overall, we identify that the susceptibility of immune cells to ferroptosis is governed by their cellular lipid composition. This work establishes the foundation for future in vivo work and promising therapeutic approaches for diseases associated with ferroptosis and immune cells.