ArticleeLife2018
Long-term antigen exposure irreversibly modifies metabolic requirements for T cell function.
Article in eLife, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
32 citing papers in PubMed, 51 citations in OpenAlex.
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- Pre-Treatment HBV Activation Modulates Circulating Immune Markers in Hepatocellular Carcinoma Patients Undergoing TACE Plus ICIs and Anti-VEGF Antibodies/TKIs.Cancer management and research · 2026Article
- Paired snRNA-seq and scRNA-seq analysis of MASLD patients to identify early-stage markers for disease progression.Hepatology communications · 2025Article
- Mitochondria reactive oxygen species signaling-dependent immune responses in macrophages and T cells.Immunity · 2025Review
- Analysis of the clinical value and influencing factors of combined detection of tuberculosis-specific cytokines IFN-γ and IL-2 in the diagnosis of active tuberculosis in children and adolescents.European journal of medical research · 2025Article
- Unravelling the Connection Between Energy Metabolism and Immune Senescence/Exhaustion in Patients with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome.Biomolecules · 2025Review
- Transcriptional reprogramming primes CD8+ T cells toward exhaustion in Myalgic encephalomyelitis/chronic fatigue syndrome.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Multiomic profiling of chronically activated CD4+ T cells identifies drivers of exhaustion and metabolic reprogramming.PLoS biology · 2024Article
- Intersection of Immunology and Metabolism in Myocardial Disease.Circulation research · 2024Review
- Expression of the monocarboxylate transporter MCT1 is required for virus-specific mouse CD8Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Actives from the Micro-Immunotherapy Medicine 2LMIREGJournal of inflammation research · 2024Article
- Surveying the Metabolic and Dysfunctional Profiles of T Cells and NK Cells in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome.International journal of molecular sciences · 2023Review
- Altered Fatty Acid Oxidation in Lymphocyte Populations of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome.International journal of molecular sciences · 2023Article
- IFNγ signaling in cytotoxic T cells restricts anti-tumor responses by inhibiting the maintenance and diversity of intra-tumoral stem-like T cells.Nature communications · 2023Article
- Reactive oxygen species formation and its effect on CD4Frontiers in immunology · 2023Review
- Chimeric antigen receptor-T cells are effective against CEACAM5 expressing non-small cell lung cancer cells resistant to antibody-drug conjugates.Frontiers in oncology · 2023Article
- Oxidative stress genes define two subtypes of triple-negative breast cancer with prognostic and therapeutic implications.Frontiers in genetics · 2023Article
- Redox regulation of the immune response.Cellular & molecular immunology · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
Abstract
Energy metabolism is essential for T cell function. However, how persistent antigenic stimulation affects T cell metabolism is unknown. Here, we report that long-term in vivo antigenic exposure induced a specific deficit in numerous metabolic enzymes. Accordingly, T cells exhibited low basal glycolytic flux and limited respiratory capacity. Strikingly, blockade of inhibitory receptor PD-1 stimulated the production of IFNγ in chronic T cells, but failed to shift their metabolism towards aerobic glycolysis, as observed in effector T cells. Instead, chronic T cells appeared to rely on oxidative phosphorylation (OXPHOS) and fatty acid oxidation (FAO) to produce ATP for IFNγ synthesis. Check-point blockade, however, increased mitochondrial production of superoxide and reduced viability and effector function. Thus, in the absence of a glycolytic switch, PD-1-mediated inhibition appears essential for limiting oxidative metabolism linked to effector function in chronic T cells, thereby promoting survival and functional fitness.
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What OpenQuestion holds
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.