ArticleCell death and differentiation2013
T-cell death following immune activation is mediated by mitochondria-localized SARM.
Article in Cell death and differentiation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
52 citing papers in PubMed, 84 citations in OpenAlex.
- Article
- Quantification of SARM1 NADase Activity in Human Peripheral Blood Mononuclear Cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Caspase-3 cleaves and activates the NADase SARM1 to promote apoptosis, linking two cell death mechanisms.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Targeting SARM1 as a novel neuroprotective therapy in neurotropic viral infections.Journal of neuroinflammation · 2025Article
- SARM regulates cell apoptosis and inflammation during Toxoplasma gondii infection through a multistep mechanism.Parasites & vectors · 2025Article
- SARM1: a key multifaceted component in immunoregulation, inflammation and neurodegeneration.Frontiers in immunology · 2025Review
- SARM1 in the pathogenesis of immune-related disease.Toxicology research · 2024Review
- Nicotinamide N-Methyltransferase (NNMT): A New Hope for Treating Aging and Age-Related Conditions.Metabolites · 2024Review
- An axon-T cell feedback loop enhances inflammation and axon degeneration.Cell reports · 2024Article
- Roles of NADCold Spring Harbor perspectives in medicine · 2024Review
- Deubiquitination of SARM1 by USP13 regulates SARM1 activation and axon degeneration.Life medicine · 2023Article
- Targeting NADFrontiers in immunology · 2023Review
- SARM suppresses TRIF, TRAF3, and IRF3/7 mediated antiviral signaling in large yellow croakerFrontiers in immunology · 2022Article
- SARM1 Promotes Photoreceptor Degeneration in an Oxidative Stress Model of Retinal Degeneration.Frontiers in neuroscience · 2022Article
- Multifaceted roles of SARM1 in axon degeneration and signaling.Frontiers in cellular neuroscience · 2022Review
- NAD+-consuming enzymes in immune defense against viral infection.The Biochemical journal · 2021Review
- Prognostic Biomarker-Based Identification of Drugs for Managing the Treatment of Endometrial Cancer.Molecular diagnosis & therapy · 2021Article
- NADNature reviews. Molecular cell biology · 2021Review
- Baseline Characteristics of Mitochondrial DNA and Mutations Associated With Short-Term Posttreatment CD4+T-Cell Recovery in Chinese People With HIV.Frontiers in immunology · 2021Article
- NADFrontiers in molecular biosciences · 2021Review
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Following acute-phase infection, activated T cells are terminated to achieve immune homeostasis, failure of which results in lymphoproliferative and autoimmune diseases. We report that sterile α- and heat armadillo-motif-containing protein (SARM), the most conserved Toll-like receptors adaptor, is proapoptotic during T-cell immune response. SARM expression is significantly reduced in natural killer (NK)/T lymphoma patients compared with healthy individuals, suggesting that decreased SARM supports NK/T-cell proliferation. T cells knocked down of SARM survived and proliferated more significantly compared with wild-type T cells following influenza infection in vivo. During activation of cytotoxic T cells, the SARM level fell before rising, correlating inversely with cell proliferation and subsequent T-cell clearance. SARM knockdown rescued T cells from both activation- and neglect-induced cell deaths. The mitochondria-localized SARM triggers intrinsic apoptosis by generating reactive oxygen species and depolarizing the mitochondrial potential. The proapoptotic function is attributable to the C-terminal sterile alpha motif and Toll/interleukin-1 receptor domains. Mechanistically, SARM mediates intrinsic apoptosis via B cell lymphoma-2 (Bcl-2) family members. SARM suppresses B cell lymphoma-extra large (Bcl-xL) and downregulates extracellular signal-regulated kinase phosphorylation, which are cell survival effectors. Overexpression of Bcl-xL and double knockout of Bcl-2 associated X protein and Bcl-2 homologous antagonist killer substantially reduced SARM-induced apoptosis. Collectively, we have shown how T-cell death following infection is mediated by SARM-induced intrinsic apoptosis, which is crucial for T-cell homeostasis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.