ArticleJournal of immunology (Baltimore, Md. : 1950)2012
Anergic CD8+ T lymphocytes have impaired NF-κB activation with defects in p65 phosphorylation and acetylation.
Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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.
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.
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Who cites it
31 citing papers in PubMed, 37 citations in OpenAlex.
- CAR design equips diverse immune cells with unique antigen-specific activation identities.Molecular therapy. Oncology · 2026Article
- The diversity of CD8Nature reviews. Immunology · 2025Review
- A mechanistic quantitative systems pharmacology model platform for translational efficacy evaluation and checkpoint combination design of bispecific immuno-modulatory antibodies.Frontiers in pharmacology · 2025Article
- Peroxisome Proliferator-Activated Receptor δ Suppresses the Cytotoxicity of CD8+ T Cells by Inhibiting RelA DNA-Binding Activity.Cancer research communications · 2024Article
- NF-κB subunits RelA and c-Rel selectively control CD4+ T cell function in multiple sclerosis and cancer.The Journal of experimental medicine · 2024Article
- Key oncogenic signaling pathways affecting tumor-infiltrating lymphocytes infiltration in hepatocellular carcinoma: basic principles and recent advances.Frontiers in immunology · 2024Review
- RELA tunes innate-like interferon I/III responses in human T cells.The Journal of experimental medicine · 2023Article
- HMOX1 pathway signature predicts clinical benefit from immunotherapy plus tyrosine kinase inhibitor therapy in advanced renal cell carcinoma.Cancer medicine · 2023Article
- Calf Thymus Polypeptide Restrains the Growth of Colorectal TumorFrontiers in pharmacology · 2022Article
- HDAC5 modulates PD-L1 expression and cancer immunity via p65 deacetylation in pancreatic cancer.Theranostics · 2022Article
- Article
- Tumor Extracellular Matrix Stiffness Promptly Modulates the Phenotype and Gene Expression of Infiltrating T Lymphocytes.International journal of molecular sciences · 2021Article
- Dietary Anti-Aging Polyphenols and Potential Mechanisms.Antioxidants (Basel, Switzerland) · 2021Review
- NF-κB in Cancer Immunity: Friend or Foe?Cells · 2021Review
- The Diverse Roles of Heme Oxygenase-1 in Tumor Progression.Frontiers in immunology · 2021Review
- Regulation of PD-L1 Expression by NF-κB in Cancer.Frontiers in immunology · 2020Review
- Chemoresistance in Breast Cancer Patients Associated With Changes in P2X7 and A2A Purinergic Receptors in CD8Frontiers in pharmacology · 2020Article
- Repurposing Tin Mesoporphyrin as an Immune Checkpoint Inhibitor Shows Therapeutic Efficacy in Preclinical Models of Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2018Article
- NF-kappaB: Two Sides of the Same Coin.Genes · 2018Review
- Activation of HIV-1 expression in latently infected CD4+ T cells by the small molecule PKC412.Virology journal · 2016Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Because of the cytotoxic potential of CD8(+) T cells, maintenance of CD8(+) peripheral tolerance is extremely important. A major peripheral tolerance mechanism is the induction of anergy, a refractory state in which proliferation and IL-2 production are inhibited. We used a TCR transgenic mouse model to investigate the signaling defects in CD8(+) T cells rendered anergic in vivo. In addition to a previously reported alteration in calcium/NFAT signaling, we also found a defect in NF-κB-mediated gene transcription. This was not due to blockade of early NF-κB activation events, including IκB degradation and NF-κB nuclear translocation, as these occurred normally in tolerant T cells. However, we discovered that anergic cells failed to phosphorylate the NF-κB p65 subunit at Ser(311) and also failed to acetylate p65 at Lys(310). Both of these modifications have been implicated as critical for NF-κB transactivation capacity, and thus, our results suggest that defects in key phosphorylation and acetylation events are important for the inhibition of NF-κB activity (and subsequent T cell function) in anergic CD8(+) T cells.
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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.