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T cell lipid peroxidation induces ferroptosis and prevents immunity to infection
Open accessAbstract
The selenoenzyme glutathione peroxidase 4 (Gpx4) is a major scavenger of phospholipid hydroperoxides. Although Gpx4 represents a key component of the reactive oxygen species-scavenging network, its relevance in the immune system is yet to be defined. Here, we investigated the importance of Gpx4 for physiological T cell responses by using T cell–specific Gpx4-deficient mice. Our results revealed that, despite normal thymic T cell development, CD8+ T cells from TΔGpx4/ΔGpx4 mice had an intrinsic defect in maintaining homeostatic balance in the periphery. Moreover, both antigen-specific CD8+ and CD4+ T cells lacking Gpx4 failed to expand and to protect from acute lymphocytic choriomeningitis virus and Leishmania major parasite infections, which were rescued with diet supplementation of high dosage of vitamin E. Notably, depletion of the Gpx4 gene in the memory phase of viral infection did not affect T cell recall responses upon secondary infection. Ex vivo, Gpx4-deficient T cells rapidly accumulated membrane lipid peroxides and concomitantly underwent cell death driven by ferroptosis but not necroptosis. These studies unveil an essential role of Gpx4 for T cell immunity.
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“the inducible or tissue-specific ablation of Gpx4 in mice provokes a variety of pathological conditions, including acute renal or hepatic injury [547, 563, 589], neurodegeneration [550, 590, 591], and defective immunity to infection [567], all of which can be prevented or mitigated by ferroptosis-inhibiting strategies.”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [567]
In the citing paper
“GPX4 is essential for the survival and expansion of recently activated T cells, indicating the importance of preventing lipid peroxidation and of iron dysregulation resulting in ferroptosis, in T cell proliferation (Matsushita et al., 2015).”
From The Role of Iron Regulation in Immunometabolism and Immune-Related Disease (2019) · cites this paper as Matsushita et al., 2015
In the citing paper
“GPX4 is essential for the survival and expansion of recently activated T cells, indicating the importance of preventing lipid peroxidation and of iron dysregulation resulting in ferroptosis, in T cell proliferation (Matsushita et al., 2015).”
From The Role of Iron Regulation in Immunometabolism and Immune-Related Disease (2019) · cites this paper as Matsushita et al., 2015
In the citing paper
“Gpx4 exerts important effects on the immune system as it is crucial for the survival of CD8+ T cells and for the expansion of both CD4+ and CD8+ T cells upon T cell receptor triggering in response to infection by preventing membrane lipid peroxidation and ferroptosis”
From Iron in immune cell function and host defense (2021) · cites this paper as [112]
In the citing paper
“and high levels of reactive oxygen species in T cells impair cytotoxicity, perhaps mediated by T cell lipid peroxidation, resulting in failure to control viruses (Henson et al. 2014; Matsushita et al. 2015).”
From Is immunosenescence influenced by our lifetime “dose” of exercise? (2016) · cites this paper as Matsushita et al. 2015
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Xu, J., Guo, Y., Wang, B., Xie, Y.-Y., Hao, M.-Y., Li, H., Han, H.-S., Li, Y., & Wu, D. (2025) · Cellular Signalling · doi:10.1016/j.cellsig.2025.112293 · Cited by 2
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Redundant or resilient? A systems view of ferroptosis surveillance mechanisms
Liang, D., & Jiang, X. (2026) · Cell chemical biology · doi:10.1016/j.chembiol.2025.11.013 · Cited by 2
Dar, M. J., Huston, R. H., Purayil, N., Cronin, A. I., Gondal, S. A., Nakhasi, H. L., Brito, R., Gannavaram, S., & Satoskar, A. R. (2026) · Redox Biology · doi:10.1016/j.redox.2026.104071 · Cited by 2
“These T cells fail to expand and mediate protective immunity upon infection [36].”
Immune Aging as a Failure of Programmed Cell Death Coordination
Lee, H.-M., Kim, E.-J., Hasan, A., & Kang, T. (2026) · International Journal of Molecular Sciences · doi:10.3390/ijms27031554 · Cited by 3
“T cells depend on strictly controlled redox signaling for activation, proliferation, and survival [162].”
Redox sensor NPGPx restrains ZAP70 activity and modulates T cell homeostasis
Su, F., Huang, S., Wei, P., Hsu, P., Li, J., Su, L., Hsieh, Y.-L., Hu, C., Hsu, J., Yang, C., et al. (2021) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2021.01.013 · Cited by 2
Camacho-Moll, M. E., Sampayo‐Reyes, A., Castorena‐Torres, F., Lozano-Garza, G., Alarcón-Galván, G., Hernández, A., Marcos, R., Alcocer-González, J. M., Támez-Guerra, R., & de León, M. B. (2021) · Molecules · doi:10.3390/molecules26185614 · Cited by 2
Enfeksiyon Hastalıklarında Ferroptozun Rolü
Işkın, A. E., & Budak, F. (2023) · Uludağ Üniversitesi Tıp Fakültesi Dergisi · doi:10.32708/uutfd.1337979 · Cited by 2
Ferroptosis - a link between iron biology, aging and COVID-19?
Čepelak, I., & Dodig, S. (2022) · Rad Hrvatske akademije znanosti i umjetnosti Medicinske znanosti · doi:10.21857/yk3jwhn429 · Cited by 2
Lipotoxicity as a Barrier for T Cell-Based Therapies
Loschinski, R., Saborido, J. R., Böttcher, M., Kahlfuß, S., & Mougiakakos, D. (2022) · Biomolecules · doi:10.3390/biom12091182 · Cited by 2
Ferroptosis Is a Potential Therapeutic Target for Pulmonary Infectious Diseases
Zhang, Y., Qian, D., Bai, X., & Sun, S. (2023) · Cellular Microbiology · doi:10.1155/2023/3875897 · Cited by 2
Guo, X., Feng, X., Yang, Y., An, W., & Bai, L. (2024) · Aging · doi:10.18632/aging.205875 · Cited by 2
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“And lots of researches have shown that GPX4 is related to the development process of human diseases (Friedmann Angeli et al., 2014; Matsushita et al., 2015).”
BackgroundMudgal, V., Garg, A. K., Dass, R. S., & Rawat, M. (2022) · Biological Trace Element Research · doi:10.1007/s12011-022-03122-9 · Cited by 1
“remain indicative of reduced oxidative stress and thus booster for health and immunity [80].”
BackgroundZheng, D., Chu, T., Yang, D., Liang, S., Yang, L., Yang, Y., Zhang, K., & Ma, W. (2025) · Advanced Biology · doi:10.1002/adbi.202500460 · Cited by 3
Li, Y., Qian, T., Han, Z., Wang, C., Zhang, M. X., Huang, C., Gu, Q., Zhang, S., Lin, Y., Wang, J., et al. (2026) · Frontiers in Oncology · doi:10.3389/fonc.2026.1767384 · Cited by 1
“In the model of speci fi c knockout of GPX4 in T cells, these cells will quickly accumulate lipid peroxide in their membranes and cause ferroptosis (161).”
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Wang, J., Liu, C., HUANG, H., Osella, S., Ai, S., Zhang, Y., Yang, J., Chen, J., & He, F. (2026) · European Journal of Medicinal Chemistry · doi:10.1016/j.ejmech.2026.118880 · Cited by 1
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“…Ferroptosis: When T cells encounter severe organellar stress, such as excessive activation of lipid peroxidation or disruption of ER calcium homeostasis, they do not persist in a functionally suppressed state but are instead physically eliminated via apoptosis or ferroptosis pathways [ 44, 45 ].”
Zemnou, C. T., & Ngakam, R. (2026) · Journal of Bio-X Research · doi:10.34133/jbioxresearch.0089 · Cited by 2
Liu, Y., Yin, L., Zhang, P., & Li, W. (2026) · Frontiers in Immunology · doi:10.3389/fimmu.2026.1825000 · Cited by 2
“Ferroptosis is not only a pathological cell-death mechanism; it is also linked to immune-cell function, in fl ammatory regulation, host defense, anti-tumor immunity, redox signaling, and tissue stress responses (159 – 161).”
Ferroptosis in the tumor immune microenvironment: A double-edged sword in immunotherapy
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Cell death mechanisms in sepsis-associated adaptive immune dysfunction
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“Finally, salidroside inhibits DOX-induced cardiomyopathy by regulating ferroptosis-dependent pathways [202]. α -tocopherol ( α -Toc), a well-known antioxidant, can effectively prevent lipid peroxidation and alleviate DOX-induced cardiotoxicity [203 – 206].”
Integrated Model Linking Hemolysis, NETosis, Ferroptosis, Lysosomal Dysfunction, and DIC in Sepsis
Iba, T., Maier, C. L., Ferrer, R., Nagaoka, I., Wada, H., & Levy, J. H. (2026) · Seminars in Thrombosis and Hemostasis · doi:10.1055/a-2920-1243 · Cited by 1
Ten controversies defining the boundaries of ferroptosis
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Ferroptosis in T cells: mechanisms, biology and translational opportunities
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Regulatory mechanism of ferroptosis, a new mode of cell death
Liu, D., Li, G., Jia, A., Zhao, Y., Cao, C., & Xing, X. (2019) · Tropical Journal of Pharmaceutical Research · doi:10.4314/tjpr.v17i11.29 · Cited by 1
“Other experiments showed that butylated hydroxytoluene, TROLOX, ebselen, αtocopherol, vitamin E [32], lysosome activity inhibitors such as lostoxin A, pepstatin methyl ester, and ammonium chloride (NH4CL) [33] inhibit ferroptosis by inhibiting lipid peroxidation.”
BackgroundJiang, S., & Xie, Y. (2019) · Springer eBooks · doi:10.1007/978-3-030-26780-3_14 · Cited by 1
Mitigating viral invasion: mTORC2’s role in neuroprotection and immunity
Volety, I., Patil, C. D., & Shukla, D. (2023) · Elsevier eBooks · doi:10.1016/b978-0-12-817558-3.00008-1 · Cited by 1
Yan, R., Chen, S., Lang, X.-L., Liu, J., & Zhou, T. (2024) · Biomedical Reports · doi:10.3892/br.2024.1894 · Cited by 1
Adaptive immunity and metabolism
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Metadata
- Authors
- Matsushita, M., Freigang, S., Schneider, C., Conrad, M., Bornkamm, G. W., & Kopf, M.
- Affiliations
- ETH Zurich (CH)
- Helmholtz Munich (DE)
- Molecular Biomedicine, Institute of Molecular Health Science, Department of Biology, ETH Zurich, 8093 Zurich, Switzerland 1
- Venue
- Journal of Experimental Medicine
- Publisher
- Rockefeller University Press
- Published
- 2015-03-30
- Volume
- 212
- Issue
- 4
- Pages
- 555-568
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- PMC
- PMC4387287
- OpenAlex
- W2065934830
- Cited by
- 672
- References
- 57
- Citations by year
- 2026: 65 · 2025: 77 · 2024: 90 · 2023: 90 · 2022: 95 · 2021: 92 · 2020: 56 · 2019: 28 · 2018: 25 · 2017: 22 · 2016: 24 · 2015: 8
- FWCI
- 12.96
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Experimental Medicine (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- Repository for Publications and Research Data (ETH Zurich) (publishedVersion, cc-by-nc-sa)
- Bern Open Repository and Information System (University of Bern) (submittedVersion, cc-by-nc-sa)
- Site cant be reached (submittedVersion)
- PuSH - Publication Server of Helmholtz Zentrum München (submittedVersion)
- ETH Zürich Research Collection
- Funders
- Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (141175, 310030B_141175/1)
- National Institutes of Health
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Ferroptosis and cancer prognosis
- Health Sciences › Nursing › Nutrition and Dietetics › Selenium in Biological Systems
- Keywords
- GPX4, ferroptosis, lipid peroxidation, T cell immunity, CD8+ T cells, CD4+ T cells, phospholipid hydroperoxides, vitamin E, lymphocytic choriomeningitis virus, Leishmania major, antiviral immunity, antiparasitic immunity, T cell homeostasis, T cell-specific knockout mice
- MeSH terms
- Phospholipid Hydroperoxide Glutathione Peroxidase, Animals, Cell Membrane, Glutathione Peroxidase, Immunologic Memory, Lymphocytic Choriomeningitis, Lymphocytic choriomeningitis virus, Thymus Gland, Vitamin E, Vitamins, Lipid Peroxidation, CD4-Positive T-Lymphocytes, Leishmaniasis, Cutaneous, Cell Death, Leishmania major, Mice, Knockout, CD8-Positive T-Lymphocytes, Mice
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