ArticleProceedings of the National Academy of Sciences of the United States of America2012
T cell receptor/CARMA1/NF-κB signaling controls T-helper (Th) 17 differentiation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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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
43 citing papers in PubMed, 55 citations in OpenAlex.
- Molecular Signature and miRNA Pattern of CD4 + T Lymphocytes in Plaque Psoriasis.Clinical reviews in allergy & immunology · 2026Review
- Extracellular vesicles from glycolytic mesenchymal stromal cells restrain arthritis progression via IL-10-Producing T and B cells.Theranostics · 2026Article
- Natural flavonoids in multiple sclerosis: molecular insights and emerging therapeutic strategies.Frontiers in immunology · 2026Review
- NF-κB in inflammation and cancer.Cellular & molecular immunology · 2025Review
- Targeting inflammation in cancer therapy: from mechanistic insights to emerging therapeutic approaches.Journal of translational medicine · 2025Review
- The NF-κB signaling network in the life of T cells.Frontiers in immunology · 2025Review
- MYC is in the CARDs: CBM complexes coordinate immune and MYC-dependent cellular function.Frontiers in molecular medicine · 2025Article
- PDIA3 orchestrates effector T cell program by serving as a chaperone to facilitate the non-canonical nuclear import of STAT1 and PKM2.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- NF-κB in biology and targeted therapy: new insights and translational implications.Signal transduction and targeted therapy · 2024Review
- RETRACTED: Secukinumab and Black Garlic Downregulate OPG/RANK/RANKL Axis and Devitalize Myocardial Interstitial Fibrosis Induced by Sunitinib in Experimental Rats.Life (Basel, Switzerland) · 2023Article
- The small molecule inhibitor BX-795 uncouples IL-2 production from inhibition of Th2 inflammation and induces CD4Frontiers in immunology · 2023Article
- Article
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- Epigenetic regulation of natural killer cell memory.Immunological reviews · 2022Review
- CD5 Controls Gut Immunity by Shaping the Cytokine Profile of Intestinal T Cells.Frontiers in immunology · 2022Article
- NF-κB signaling in inflammation and cancer.MedComm · 2021Review
- NF-κB regulation in maternal immunity during normal and IUGR pregnancies.Scientific reports · 2021Article
- Blockade of NF-κB Translocation and of RANKL/RANK Interaction Decreases the Frequency of Th2 and Th17 Cells Capable of IL-4 and IL-17 Production, Respectively, in a Mouse Model of Allergic Asthma.Molecules (Basel, Switzerland) · 2021Article
- NF-κB: At the Borders of Autoimmunity and Inflammation.Frontiers in immunology · 2021Review
- Association between the pig genome and its gut microbiota composition.Scientific reports · 2019Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
IL-17-producing CD4 T cells play a key role in immune responses against extracellular bacteria and autoimmunity. Nuclear factor κB (NF-κB) is required for T-cell activation and selected effector functions, but its role in Th17 differentiation is controversial. Using genetic mouse models that impede T-cell-NF-κB signaling either downstream of the T-cell receptor (TCR) or of IκB kinase β (IKKβ), we demonstrate that NF-κB signaling controls not only survival and proliferation of activated T cells, but, if cell survival and cell-cycle progression are enabled, has an additional role in promoting completion of Th17 differentiation. CARD-containing MAGUK protein 1 (CARMA1), an adapter required for TCR/NF-κB signaling, was necessary for acquisition of IL-17A, IL-17F, IL-21, IL-22, IL-23R, and CCR6 expression in T cells cultured under Th17 conditions. In proliferating cells, lack of CARMA1 selectively prevented Th17, but not Th1 or Th2 differentiation, in a cell-intrinsic manner. Consistent with these data, CARMA1-KO mice were resistant to experimental autoimmune encephalomyelitis. Surprisingly, transcription factors essential for Th17 differentiation such as RORγt, AHR, and IRF4 were normally induced in CARMA1-KO T cells activated under Th17 conditions, suggesting that the Th17 differentiation program was initiated normally. Instead, chromatin loci of Th17 effector molecules failed to acquire an open conformation in CARMA1-KO T cells. Our results demonstrate that TCR/CARMA1/NF-κB controls completion of Th17 differentiation by enabling chromatin accessibility of Th17 effector molecule loci.
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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.