Abstract
The cellular lipidome comprises thousands of unique lipid species. Here, using mass spectrometry-based targeted lipidomics, we characterize the lipid landscape of human and mouse immune cells (www.cellularlipidatlas.com). Using this resource, we show that immune cells have unique lipidomic signatures and that processes such as activation, maturation and development impact immune cell lipid composition. To demonstrate the potential of this resource to provide insights into immune cell biology, we determine how a cell-specific lipid trait—differences in the abundance of polyunsaturated fatty acid-containing glycerophospholipids (PUFA-PLs)—influences immune cell biology. First, we show that differences in PUFA-PL content underpin the differential susceptibility of immune cells to ferroptosis. Second, we show that low PUFA-PL content promotes resistance to ferroptosis in activated neutrophils. In summary, we show that the lipid landscape is a defining feature of immune cell identity and that cell-specific lipid phenotypes underpin aspects of immune cell physiology.
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Data availability
All of the data supporting the findings of this study are available from the corresponding author upon reasonable request. All of the lipidomic datasets are available in Figshare (https://doi.org/10.26180/25217357.v2). Source data are provided with this paper.
References
Harayama, T. & Riezman, H. Understanding the diversity of membrane lipid composition. Nat. Rev. Mol. Cell Biol. 19, 281–296 (2018).
Holthuis, J. C. & Menon, A. K. Lipid landscapes and pipelines in membrane homeostasis. Nature 510, 48–57 (2014).
Storck, E. M., Ozbalci, C. & Eggert, U. S. Lipid cell biology: a focus on lipids in cell division. Annu. Rev. Biochem. 87, 839–869 (2018).
Zhang, Q. et al. Biosynthesis and roles of phospholipids in mitochondrial fusion, division and mitophagy. Cell. Mol. Life Sci. 71, 3767–3778 (2014).
Walpole, G. F. W. & Grinstein, S. Endocytosis and the internalization of pathogenic organisms: focus on phosphoinositides. F1000Res 9, 368 (2020).
Sezgin, E., Levental, I., Mayor, S. & Eggeling, C. The mystery of membrane organization: composition, regulation and roles of lipid rafts. Nat. Rev. Mol. Cell Biol. 18, 361–374 (2017).
Morioka, S., Maueroder, C. & Ravichandran, K. S. Living on the edge: efferocytosis at the interface of homeostasis and pathology. Immunity 50, 1149–1162 (2019).
Jiang, X., Stockwell, B. R. & Conrad, M. Ferroptosis: mechanisms, biology and role in disease. Nat. Rev. Mol. Cell Biol. 22, 266–282 (2021).
Chen, B., Sun, Y., Niu, J., Jarugumilli, G. K. & Wu, X. Protein lipidation in cell signaling and diseases: function, regulation, and therapeutic opportunities. Cell Chem. Biol. 25, 817–831 (2018).
Verkerke, A. R. P. & Kajimura, S. Oil does more than light the lamp: the multifaceted role of lipids in thermogenic fat. Dev. Cell 56, 1408–1416 (2021).
Li, H. et al. The landscape of cancer cell line metabolism. Nat. Med. 25, 850–860 (2019).
Surma, M. A. et al. Mouse lipidomics reveals inherent flexibility of a mammalian lipidome. Sci. Rep. 11, 19364 (2021).
Alarcon-Barrera, J. C. et al. Lipid metabolism of leukocytes in the unstimulated and activated states. Anal. Bioanal. Chem. 412, 2353–2363 (2020).
Liew, P. X. & Kubes, P. The neutrophil’s role during health and disease. Physiol. Rev. 99, 1223–1248 (2019).
Hannun, Y. A. & Obeid, L. M. Sphingolipids and their metabolism in physiology and disease. Nat. Rev. Mol. Cell Biol. 19, 175–191 (2018).
Han, G. et al. Identification of small subunits of mammalian serine palmitoyltransferase that confer distinct acyl-CoA substrate specificities. Proc. Natl Acad. Sci. USA 106, 8186–8191 (2009).
Karsai, G. et al. FADS3 is a Δ14Z sphingoid base desaturase that contributes to gender differences in the human plasma sphingolipidome. J. Biol. Chem. 295, 1889–1897 (2020).
Patel, A. A. et al. The fate and lifespan of human monocyte subsets in steady state and systemic inflammation. J. Exp. Med. 214, 1913–1923 (2017).
Evrard, M. et al. Developmental analysis of bone marrow neutrophils reveals populations specialized in expansion, trafficking, and effector functions. Immunity 48, 364–379.e8 (2018).
Kagan, V. E. et al. Oxidized arachidonic and adrenic PEs navigate cells to ferroptosis. Nat. Chem. Biol. 13, 81–90 (2017).
Zou, Y. et al. Plasticity of ether lipids promotes ferroptosis susceptibility and evasion. Nature 585, 603–608 (2020).
Xu, L., Davis, T. A. & Porter, N. A. Rate constants for peroxidation of polyunsaturated fatty acids and sterols in solution and in liposomes. J. Am. Chem. Soc. 131, 13037–13044 (2009).
Yin, H., Xu, L. & Porter, N. A. Free radical lipid peroxidation: mechanisms and analysis. Chem. Rev. 111, 5944–5972 (2011).
Bersuker, K. et al. The CoQ oxidoreductase FSP1 acts parallel to GPX4 to inhibit ferroptosis. Nature 575, 688–692 (2019).
Doll, S. et al. FSP1 is a glutathione-independent ferroptosis suppressor. Nature 575, 693–698 (2019).
Soula, M. et al. Metabolic determinants of cancer cell sensitivity to canonical ferroptosis inducers. Nat. Chem. Biol. 16, 1351–1360 (2020).
Mao, C. et al. DHODH-mediated ferroptosis defence is a targetable vulnerability in cancer. Nature 593, 586–590 (2021).
Doll, S. et al. ACSL4 dictates ferroptosis sensitivity by shaping cellular lipid composition. Nat. Chem. Biol. 13, 91–98 (2017).
Drijvers, J. M. et al. Pharmacologic screening identifies metabolic vulnerabilities of CD8+ T cells. Cancer Immunol. Res. 9, 184–199 (2021).
Kraft, V. A. N. et al. GTP cyclohydrolase 1/tetrahydrobiopterin counteract ferroptosis through lipid remodeling. ACS Cent. Sci. 6, 41–53 (2020).
Yang, W. S. et al. Peroxidation of polyunsaturated fatty acids by lipoxygenases drives ferroptosis. Proc. Natl Acad. Sci. USA 113, E4966–E4975 (2016).
Canli, O. et al. Myeloid cell-derived reactive oxygen species induce epithelial mutagenesis. Cancer Cell 32, 869–883.e5 (2017).
Jia, M. et al. Redox homeostasis maintained by GPX4 facilitates STING activation. Nat. Immunol. 21, 727–735 (2020).
Matsushita, M. et al. T cell lipid peroxidation induces ferroptosis and prevents immunity to infection. J. Exp. Med. 212, 555–568 (2015).
Xu, C. et al. The glutathione peroxidase Gpx4 prevents lipid peroxidation and ferroptosis to sustain Treg cell activation and suppression of antitumor immunity. Cell Rep. 35, 109235 (2021).
Ramesha, C. S. & Pickett, W. C. Fatty acid composition of diacyl, alkylacyl, and alkenylacyl phospholipids of control and arachidonate-depleted rat polymorphonuclear leukocytes. J. Lipid Res. 28, 326–331 (1987).
Mueller, H. W., O’Flaherty, J. T. & Wykle, R. L. Ether lipid content and fatty acid distribution in rabbit polymorphonuclear neutrophil phospholipids. Lipids 17, 72–77 (1982).
Paul, S., Lancaster, G. I. & Meikle, P. J. Plasmalogens: a potential therapeutic target for neurodegenerative and cardiometabolic disease. Prog. Lipid Res. 74, 186–195 (2019).
Dean, J. M. & Lodhi, I. J. Structural and functional roles of ether lipids. Protein Cell 9, 196–206 (2018).
Albert, C. J., Crowley, J. R., Hsu, F. F., Thukkani, A. K. & Ford, D. A. Reactive brominating species produced by myeloperoxidase target the vinyl ether bond of plasmalogens: disparate utilization of sodium halides in the production of α-halo fatty aldehydes. J. Biol. Chem. 277, 4694–4703 (2002).
Albert, C. J. et al. Eosinophil peroxidase-derived reactive brominating species target the vinyl ether bond of plasmalogens generating a novel chemoattractant, α-bromo fatty aldehyde. J. Biol. Chem. 278, 8942–8950 (2003).
Thukkani, A. K. et al. Reactive chlorinating species produced during neutrophil activation target tissue plasmalogens: production of the chemoattractant, 2-chlorohexadecanal. J. Biol. Chem. 277, 3842–3849 (2002).
Lodhi, I. J. et al. Peroxisomal lipid synthesis regulates inflammation by sustaining neutrophil membrane phospholipid composition and viability. Cell Metab. 21, 51–64 (2015).
Dorninger, F., Wiesinger, C., Braverman, N. E., Forss-Petter, S. & Berger, J. Ether lipid deficiency does not cause neutropenia or leukopenia in mice and men. Cell Metab. 21, 650–651 (2015).
Ma, X. et al. CD36-mediated ferroptosis dampens intratumoral CD8+ T cell effector function and impairs their antitumor ability. Cell Metab. 33, 1001–1012.e5 (2021).
Xu, S. et al. Uptake of oxidized lipids by the scavenger receptor CD36 promotes lipid peroxidation and dysfunction in CD8+ T cells in tumors. Immunity 54, 1561–1577.e7 (2021).
Yao, Y. et al. Selenium–GPX4 axis protects follicular helper T cells from ferroptosis. Nat. Immunol. 22, 1127–1139 (2021).
Yang, W. S. et al. Regulation of ferroptotic cancer cell death by GPX4. Cell 156, 317–331 (2014).
Burn, G. L., Foti, A., Marsman, G., Patel, D. F. & Zychlinsky, A. The neutrophil. Immunity 54, 1377–1391 (2021).
Ubellacker, J. M. et al. Lymph protects metastasizing melanoma cells from ferroptosis. Nature 585, 113–118 (2020).
Nguyen, G. T., Green, E. R. & Mecsas, J. Neutrophils to the ROScue: mechanisms of NADPH oxidase activation and bacterial resistance. Front. Cell. Infect. Microbiol. 7, 373 (2017).
Weir, J. M. et al. Plasma lipid profiling in a large population-based cohort. J. Lipid Res. 54, 2898–2908 (2013).
Huynh, K. et al. High-throughput plasma lipidomics: detailed mapping of the associations with cardiometabolic risk factors. Cell Chem. Biol. 26, 71–84.e4 (2019).
Brugger, B., Erben, G., Sandhoff, R., Wieland, F. T. & Lehmann, W. D. Quantitative analysis of biological membrane lipids at the low picomole level by nano-electrospray ionization tandem mass spectrometry. Proc. Natl Acad. Sci. USA 94, 2339–2344 (1997).
Koivusalo, M., Haimi, P., Heikinheimo, L., Kostiainen, R. & Somerharju, P. Quantitative determination of phospholipid compositions by ESI-MS: effects of acyl chain length, unsaturation, and lipid concentration on instrument response. J. Lipid Res. 42, 663–672 (2001).
Fahy, E. et al. A comprehensive classification system for lipids. J. Lipid Res. 46, 839–861 (2005).
Fahy, E. et al. Update of the LIPID MAPS comprehensive classification system for lipids. J. Lipid Res. 50, S9–S14 (2009).
Liebisch, G. et al. Shorthand notation for lipid structures derived from mass spectrometry. J. Lipid Res. 54, 1523–1530 (2013).
Alshehry, Z. H. et al. An efficient single phase method for the extraction of plasma lipids. Metabolites 5, 389–403 (2015).
Deshwal, S. et al. Mitochondria regulate intracellular coenzyme Q transport and ferroptotic resistance via STARD7. Nat. Cell Biol. 25, 246–257 (2023).
Zhang, L. et al. Low-input lipidomics reveals lipid metabolism remodelling during early mammalian embryo development.Nat. Cell Biol. 26, 278–293 (2024).
Acknowledgements
We thank the members of the ARA Flow Cytometry Core Facility for expert assistance. We thank the members of ARA Animal Services who provided wonderful care of the mice used in this work. We thank all of the human volunteers who provided blood samples to assist with this work. We acknowledge staff at the facilities where the Acsl4−/− mice were generated, including those at the MAGEC laboratory who provided scientific and technical assistance. MAGEC is supported by Phenomics Australia. Phenomics Australia is supported by the Australian Government through the National Collaborative Research Infrastructure Strategy programme. We are grateful to C. Sobey for providing access to the Nox2−/− mice. Schematic figures were created using Biorender.com. We are extremely grateful to the following funding sources: National Health and Medical Research Council of Australia (grants GNT1189012 (to G.I.L.), GNT1194329 (to A.J.M.), GNT1197190 (to K.H.) and GNT2009965 (to P.J.M.)), a CSL Centenary Fellowship (to A.J.M.) and the Victorian Government’s Operational Support Program. The funders had no role in study design, data collection and analysis, decision to publish or preparation of the manuscript.
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G.I.L., A.J.M., G.P. and P.K.M. conceived of the idea. G.P., P.K.M., C.B.V., M.K.S.L., T.M.D.S., T.J.C.C. and Y.X. performed the investigation. G.P., P.K.M., A.A.T.S., C.G., G.I.L., K.H., A.L. and T.v.B.-M. performed the formal analysis. G.I.L., A.J.M., K.H., G.P., P.K.M. and M.K.S.L. developed the methodology. C.G. developed the software. G.P., P.K.M., C.G., S.P. and G.I.L. visualized the results. G.I.L. and A.J.M. acquired funding. G.I.L., A.J.M. and P.J.M. supervised the study. N.A.M. coordinated the project. G.I.L. wrote the original draft of the paper. All authors reviewed and edited the paper.
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G.I.L., A.J.M., P.J.M., S.P. and P.K.M. have filed a patent application in Australia (application no. 2023900331) relating to the composition of plasmalogens within immune cells, which forms a partial basis for the formulation of plasmalogen supplements as a nutritional way to impact cell function. The other authors declare no competing interests.
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Extended data
Extended Data Fig. 1 Changes in specific lipid features in human and mouse immune cells.
a-p, Levels of specific lipid features in human (a-c,g-j,o) and mouse (d-f,k-n,p) immune cells. Data are shown as a box and whiskers, with the lower and upper limits of the box corresponding to the 25th and 75th percentile, the line within the box being the median, and the whiskers extending to the minimum and maximum values. P values for pairwise comparisons are shown in Table S1 and Table S2. In a-c,g-j,o, the n value denoting the number of individual human donor for each cell type are as follows: 14 for naive B cells, CD4 TCM, CD8 TNaive, classical monocytes, intermediate monocytes, and basophils; 13 for Memory B cells, CD4 TNaive, CD4 TEM, CD8 TEM, non-classical monocytes, and eosinophils; 12 for CD8 TCM, CD56dim NK cells and CD56bright NK cells; 11 for neutrophils. In d-f,k-n,p, the n value denoting the number of mice for each cell type are as follows: 8 for B cells and CD8 T cells; 9 for CD4 T cells, eosinophils, Ly6Clo monocytes and NK cells; 10 for Ly6Chi monocytes and neutrophil.
Extended Data Fig. 2 Changes in alkyl/acyl composition within specific PL subclasses.
a-p, Alkyl/acyl composition for the indicated PL subclasses in human (a-h) and mouse (i-p) immune cells. Data are shown as mean + S.D and statistically significant differences in lipid features between cell types was determined by 1-way ANOVA with Tukey’s HSD test after false discovery rate correction (5%; Benjamini-Hochberg). P values for all pairwise comparisons are shown in Table S1 and Table S2. In a-h, the n value denoting the number of individual human donor for each cell type are as follows: 14 for naive B cells, CD4 TCM, CD8 TNaive, classical monocytes, intermediate monocytes, and basophils; 13 for Memory B cells, CD4 TNaive, CD4 TEM, CD8 TEM, non-classical monocytes, and eosinophils; 12 for CD8 TCM, CD56dim NK cells and CD56bright NK cells; 11 for neutrophils. In i-p, the n value denoting the number of mice for each cell type are as follows: 8 for B cells and CD8 T cells; 9 for CD4 T cells, eosinophils, Ly6Clo monocytes and NK cells; 10 for Ly6Chi monocytes and neutrophil.
Extended Data Fig. 3 Sphingolipid changes in the cells of the human and mouse immune system.
a-f, Breakdown of the indicated sphingolipid features in human (a-c) and mouse (d-f) immune cells. Data are shown as mean + S.D and statistically significant differences in lipid features between cell types was determined by 1-way ANOVA with Tukey’s HSD test after false discovery rate correction (5%; Benjamini-Hochberg). P values for all pairwise comparisons are shown in Table S1 and Table S2. In a-c, the n value denoting the number of individual human donor for each cell type are as follows: 14 for naive B cells, CD4 TCM, CD8 TNaive, classical monocytes, intermediate monocytes, and basophils; 13 for Memory B cells, CD4 TNaive, CD4 TEM, CD8 TEM, non-classical monocytes, and eosinophils; 12 for CD8 TCM, CD56dim NK cells and CD56bright NK cells; 11 for neutrophils. In d-f, the n value denoting the number of mice for each cell type are as follows: 8 for B cells and CD8 T cells; 9 for CD4 T cells, eosinophils, Ly6Clo monocytes and NK cells; 10 for Ly6Chi monocytes and neutrophil.
Extended Data Fig. 4 Human monocyte maturation status influences lipid composition.
a, Gene expression (nTPM) of Elovl1 and Elovl5 in CD4Naive and CD4Memory T cells from 6 individual donors (data from the RNA Human Protein Atlas immune cell sample gene dataset). Data are shown as mean + S.E.M and statistically significant differences were determined using a paired t-test. b, Volcano plot of lipid changes in human non-classical and classical monocytes. c-j, Changes in the indicated lipids in non-classical and classical monocytes. Data are shown as mean + S.E.M. and statistically significant differences were determined using a two-tailed unpaired t-test. n = 14 individual human donors for classical monocytes and 13 for non-classical monocytes.
Extended Data Fig. 5 Supporting data for Fig. 4.
a, Schematic of the various ferroptosis-inducing and -inhibiting compounds used. b, Cell viability of bone marrow (BM) immune cells treated with RSL3 at the indicated doses for 24 h. c, Cell viability of FACS-sorted immune cells treated with the indicated doses of RSL3 for 24 h. d-g, Cell viability and Liperfluo fluorescence in T cells (d,e) and B cells (f,g) treated with vehicle (DMSO), RSL3 (2 μM) alone, or in combination with either α-TOH (200 μM) or Fer-1 (1 μM) for 24 h. h, Cell viability of BM immune cells treated with erastin at the indicated doses for 24 h. i-l, Cell viability and Liperfluo fluorescence in T cells (i,j) and B cells (k,l) treated with vehicle (DMSO), erastin (5 μM) alone, or in combination with either α-TOH (200 μM) or Fer-1 (1 μM) for 24 h. b-l, n = 6 mice. m, Cell viability of BM monocytes treated with the indicated doses of ML210 alone or in combination with methotrexate (1.5 μM), ferroptosis suppressor protein 1 inhibitor (iFSP1; 3 μM), or methotrexate + iFSP1 for 24 h. n = 6 mice with the exception of n = 5 for methotrexate + iFSP1 with 20 μM of ML210. n,o, Cell viability (n) and Liperfluo fluorescence (o) in BM monocytes treated with vehicle (DMSO), ML210 (1 μM), iFSP1 (3 μM), or ML210 + iFSP1, in the presence of α-TOH (200 μM), idebenone (10 μM) or Fer-1 (1 μM) for 24 h. In n, n = 9 mice with the exception of n = 6 for ML210 alone and iFSP1 alone treatments; in o, n = 6 mice with the exception of n = 5 for ML210 + iFSP1 + IDB treatment. p-u, Cell viability in BM neutrophils (p) and monocytes (s) treated with brequniar (BQR) in the presence of ML210 (1 or 10 μM) or DMSO for 24 h. Liperfluo fluorescence and cell viability in BM neutrophils (q,r) and monocytes (t,u) treated with BQR (500 μM) in the presence of α-TOH (200 μM), Fer-1 (1 μM), ciclopirox (CPX) (10 μM) or DMSO for 24 h or following pre-treatment with z-VAD (25 μM) or Nec-1s (10 μM) for an hour. Data are shown as mean ± S.E.M. and was analysed using a 1-way ANOVA with Tukey’s HSD test. n = 6 mice (p-u) with the exception of n = 3 independent samples treated with 250 μM of BQR (p,s) and n = 5 independent samples treated with BQR and Fer-1 (r,u). Schematic in a created with BioRender.com.
Extended Data Fig. 6 ML210 treatment in T cells, B cells, and monocytes differentially influences phospholipid composition.
a-c, Significantly different phospholipid species in T cells (a), B cells (b) and monocytes (c) treated with vehicle (DMSO), ML210 (1 μM) or ML210 + Ferrostatin-1 (Fer-1; 1 μM) for 24 h. The phospholipid species shown are those that were significantly different (1-way ANOVA with Tukey’s HSD test) after false discovery rate correction (Benjamini-Hochberg). Data are presented as z-scores. n = 7-8 mice. d-g, Individual PUFA-containing phospholipid species in FACS-sorted T cells (d), B cells (e), monocytes (f), and neutrophils (g) treated with vehicle (DMSO), ML210 (1 μM), or ML210 (1 μM) + Ferrostatin-1 (Fer-1; 1 μM) for 24 hours. Data are shown as mean ± S.E.M. and was analysed using a 1-way ANOVA with Tukey’s HSD test. n = 8 mice (a-g) for all conditions with the exception of n = 7 for ML210 treated monocytes (c, f) and n = 7 for ML210 + Fer-1 treated neutrophils (g).
Extended Data Fig. 7 Supporting data for Fig. 6.
a-c, Percentage of PLs with the indicated number of carbon-carbon double bonds following treatment of purified T cells with either oleate [200 μM] (a; n = 6 mice) or PE(18:0/18:1) [20 μM] (b; n = 6 mice for ethanol treated samples and n = 5 mice for PE(18:0/18:1) treated samples), or in T cells purified from WT and Acsl4-/- mice (c; n = 4 mice). Data are shown as mean ± S.E.M. and was analysed using a two-tailed un-paired student’s t-test.
Extended Data Fig. 8 Supporting data for Fig. 7.
a, Percentage of PLs with the indicated number of carbon-carbon double bonds following treatment of purified neutrophils with AA + DHA at the indicated doses either in the absence or presence of Fer-1 (1 μM). b-e, Abundance of the indicated PUFAs within PLs overall (b) and within the indicated specific PL classes following treatment of purified neutrophils with AA + DHA at the indicated doses either in the absence or presence of Fer-1 (c-e). f, Cellular PL peroxidation index following treatment of purified neutrophils with AA + DHA at the indicated doses either in the absence or presence of Fer-1. g, Immunoblot of NOX2 protein expression in the WT and Nox2-/- neutrophils used in experiments described in Fig. 7. Data was analysed using either a 1-way ANOVA or 2-way ANOVA with Tukey’s HSD test. Data are shown as mean ± S.E.M from n = 6 mice.
Extended Data Fig. 9 Supporting data for Fig. 8.
a, Response of each species measured in the PC Internal Standard Mixture – UltimateSPLASH under the reported LC-MS/MS conditions. From left to right, PC(17:0_14:1)-d5, PC(17:0_16:1)-d5, PC(17:0_18:1)-d5, PC(17:0_22:4)-d5, PC(17:0_20:3)-d5. b, Comparisons between measured response, and expected response, relative to the area of PC(17:0_16:1)-d5. Expected responses were derived from concentrations provided with the PC Internal Standard Mixture – UltimateSPLASH (50-150 micrograms per mL).
Supplementary information
Supplementary information
Supplementary Figs. 1–5.
Supplementary Table 1
Significance values for all human lipid atlas data.
Supplementary Table 2
Significance values for all mouse lipid atlas data.
Supplementary Table 3
Antibody panel used for lipid atlas.
Supplementary Table 4
Mass spectrometry conditions.
Supplementary Table 5
Mass spectrometry conditions.
Supplementary Table 6
Antibody panel used for ferroptosis experiments.
Supplementary Table 7
Reagent list.
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Morgan, P.K., Pernes, G., Huynh, K. et al. A lipid atlas of human and mouse immune cells provides insights into ferroptosis susceptibility. Nat Cell Biol 26, 645–659 (2024). https://doi.org/10.1038/s41556-024-01377-z
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DOI: https://doi.org/10.1038/s41556-024-01377-z
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