ArticleThe Journal of experimental medicine2009
Transcriptional complexes formed by NFAT dimers regulate the induction of T cell tolerance.
Article in The Journal of experimental medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
51 citing papers in PubMed, 83 citations in OpenAlex.
- CD8 T Cell Sensing of Type I Interferon Impacts Anergy.European journal of immunology · 2026Article
- Virus-like antigen display delivers a stand-alone danger signal through the BCR that circumvents tolerance.bioRxiv : the preprint server for biology · 2026Article
- T Cell Resistance: On the Mechanisms of T Cell Non-activation.Immune network · 2024Review
- The CD8Immunity · 2024Article
- Review
- Molecular treatment trajectories within psoriatic T lymphocytes: a mini review.Frontiers in immunology · 2023Review
- Immune Regulatory Processes of the Tumor Microenvironment under Malignant Conditions.International journal of molecular sciences · 2021Review
- Advances in Lipid-Based Nanoparticles for Cancer Chemoimmunotherapy.Pharmaceutics · 2021Review
- Reversing Post-Infectious Epigenetic-Mediated Immune Suppression.Frontiers in immunology · 2021Review
- Tolerization of recent thymic emigrants is required to prevent RBC-specific autoimmunity.Journal of autoimmunity · 2020Article
- NFAT2 overexpression suppresses the malignancy of hepatocellular carcinoma through inducing Egr2 expression.BMC cancer · 2020Article
- Lymphopenia and lymphocytosis in practical healthy people born and living in the North.Immunity, inflammation and disease · 2020Article
- Revisiting T Cell Tolerance as a Checkpoint Target for Cancer Immunotherapy.Frontiers in immunology · 2020Review
- Accelerator or Brake: Immune Regulators in Malaria.Frontiers in cellular and infection microbiology · 2020Review
- Induction of Tolerance and Immunity by Dendritic Cells: Mechanisms and Clinical Applications.Frontiers in immunology · 2019Review
- Nanoluciferase Reporter Gene System Directed by Tandemly Repeated Pseudo-Palindromic NFAT-Response Elements Facilitates Analysis of Biological Endpoint Effects of Cellular CaInternational journal of molecular sciences · 2018Article
- NFAT control of immune function: New Frontiers for an Abiding Trooper.F1000Research · 2018Review
- NFAT2 is a critical regulator of the anergic phenotype in chronic lymphocytic leukaemia.Nature communications · 2017Article
- The Transcription Factor NFAT1 Participates in the Induction of CD4Infection and immunity · 2017Article
- NFATc2 Modulates Microglial Activation in the AβPP/PS1 Mouse Model of Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
In T cells, anergy can be induced after T cell receptor engagement in the absence of costimulation. Under these conditions, the expression of a specific set of anergy-associated genes is activated. Several lines of evidence suggest that nuclear factor of activated T cells (NFAT) proteins may regulate the expression of many of those genes; however, the nature of the complexes responsible for the induction of this new program of gene expression is unknown. Here, we show that transcriptional complexes formed by NFAT homodimers are directly responsible for the activation of at least two anergy-inducing genes, Grail and Caspase3. Our data shows that Grail expression is activated by direct binding of NFAT dimers to the Grail promoter at two different sites. Consequently, a mutant NFAT protein with impaired ability to dimerize is not able to induce an unresponsive state in T cells. Our results not only identify a new biological function for NFAT dimers but also reveal the different nature of NFAT-containing complexes that induce anergy versus those that are activated during a productive immune response. These data also establish a basis for the design of immunomodulatory strategies that specifically target each type of complex.
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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.