ArticlePLoS biology2020
Eomes broadens the scope of CD8 T-cell memory by inhibiting apoptosis in cells of low affinity.
Article in PLoS biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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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
22 citing papers in PubMed, 50 citations in OpenAlex.
- Smad4 and Eomes converge on a shared transcriptional program associated with inflammatory CD8 T-cell differentiation.Frontiers in immunology · 2026Article
- T-cell immunity against influenza virus does not require Th1 or Th17 master regulator transcription factors.Mucosal immunology · 2025Article
- CD1d-Restricted NKT Cells Promote Central Memory CD8International journal of molecular sciences · 2025Article
- GFI1-driven transcriptional and epigenetic programs maintain CD8Nature immunology · 2025Article
- NK cell-derived IFNγ mobilizes free fatty acids from adipose tissue to promote early B cell activation during viral infection.Nature metabolism · 2025Article
- DYNC2H1 mutation as a potential predictive biomarker for immune checkpoint inhibitor efficacy in NSCLC and melanoma.Investigational new drugs · 2025Article
- Low-affinity CD8American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2024Article
- Expansion of memory Vδ2 T cells following SARS-CoV-2 vaccination revealed by temporal single-cell transcriptomics.NPJ vaccines · 2024Article
- Preimmunization with Listeria-vectored cervical cancer vaccine candidate strains can establish specific T-cell immune memory and prevent tumorigenesis.BMC cancer · 2024Article
- Rethinking IL-1 Antagonism in Respiratory Viral Infections: A Role for IL-1 Signaling in the Development of Antiviral T Cell Immunity.International journal of molecular sciences · 2023Article
- Interferon-γ couples CD8Nature communications · 2023Article
- Article
- Small intestine and colon tissue-resident memory CD8Immunity · 2023Article
- T-cell exhaustion and stemness in antitumor immunity: Characteristics, mechanisms, and implications.Frontiers in immunology · 2023Review
- Comparative transcriptomes reveal pro-survival and cytotoxic programs of mucosal-associated invariant T cells upon Bacillus Calmette-Guérin stimulation.Frontiers in cellular and infection microbiology · 2023Article
- Regulation of CD4 T Cell Responses by the Transcription Factor Eomesodermin.Biomolecules · 2022Review
- Adoptive transfer of IL-4 reprogrammed Tc17 cells elicits anti-tumour immunity through functional plasticity.Immunology · 2022Article
- Divide and Conquer: Phenotypic and Temporal Heterogeneity Within CD8Frontiers in immunology · 2022Review
- Staggered starts in the race to T cell activation.Trends in immunology · 2021Review
- CD8 T Cell Vaccines and a Cytomegalovirus-Based Vector Approach.Life (Basel, Switzerland) · 2021Review
Corrections and comments
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Authors and funding
15 authors at 5 institutions in 6 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The memory CD8 T-cell pool must select for clones that bind immunodominant epitopes with high affinity to efficiently counter reinfection. At the same time, it must retain a level of clonal diversity to allow recognition of pathogens with mutated epitopes. How the level of diversity within the memory pool is controlled is unclear, especially in the context of a selective drive for antigen affinity. We find that preservation of clones that bind the activating antigen with low affinity depends on expression of the transcription factor Eomes in the first days after antigen encounter. Eomes is induced at low activating signal strength and directly drives transcription of the prosurvival protein Bcl-2. At higher signal intensity, T-bet is induced which suppresses Bcl-2 and causes a relative survival advantage for cells of low affinity. Clones activated with high-affinity antigen form memory largely independent of Eomes and have a proliferative advantage over clones that bind the same antigen with low affinity. This causes high-affinity clones to prevail in the memory pool, despite their relative survival deficit. Genetic or therapeutic targeting of the Eomes/Bcl-2 axis reduces the clonal diversity of the memory pool, which diminishes its ability to respond to pathogens carrying mutations in immunodominant epitopes. Thus, we demonstrate on a molecular level how sufficient diversity of the memory pool is established in an environment of affinity-based selection.
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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 Socratic graph.