ArticleBlood2009
Regulation of Th17 cell differentiation and EAE induction by MAP3K NIK.
Article in Blood, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 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
57 citing papers in PubMed, 90 citations in OpenAlex.
- Immunotherapy converts nonimmunogenic pancreatic tumors into immunogenic foci of immune regulation.Cancer immunology research · 2014Trial
- NF-κB in inflammation and cancer.Cellular & molecular immunology · 2025Review
- Targeting NF-kappaB-inducing kinase shapes B-cell homeostasis in myasthenia gravis.Journal of neuroinflammation · 2025Article
- BTLA agonist attenuates Th17-driven inflammation in a mouse model of steroid-resistant asthma.Frontiers in immunology · 2025Article
- The NF-κB signaling network in the life of T cells.Frontiers in immunology · 2025Review
- SMAC mimetics inhibit human T cell proliferation and fail to augment type 1 cytokine responses.Cellular immunology · 2023Article
- NF-κB in control of regulatory T cell development, identity, and function.Journal of molecular medicine (Berlin, Germany) · 2022Review
- Review
- A T cell-intrinsic function for NF-κB RelB in experimental autoimmune encephalomyelitis.Scientific reports · 2021Article
- Article
- Combined immunodeficiency with autoimmunity caused by a homozygous missense mutation in inhibitor of nuclear factor 𝛋B kinase alpha (IKKα).Science immunology · 2021Article
- Microglia promote autoimmune inflammation via the noncanonical NF-κB pathway.Science advances · 2021Article
- Targeting NF-κB pathway for the therapy of diseases: mechanism and clinical study.Signal transduction and targeted therapy · 2020Review
- Reduced IκB-α Protein Levels in Peripheral Blood Cells of Patients with Multiple Sclerosis-A Possible Cause of Constitutive NF-κB Activation.Journal of clinical medicine · 2020Article
- Review
- CD28 Individual Signaling Up-regulates Human IL-17A Expression by Promoting the Recruitment of RelA/NF-κB and STAT3 Transcription Factors on the Proximal Promoter.Frontiers in immunology · 2019Article
- CRL4The Journal of experimental medicine · 2018Article
- Regulation of Interleukin-6 Receptor Signaling by TNF Receptor-Associated Factor 2 and 5 During Differentiation of Inflammatory CD4Frontiers in immunology · 2018Review
- Constitutive expression of NF-κB inducing kinase in regulatory T cells impairs suppressive function and promotes instability and pro-inflammatory cytokine production.Scientific reports · 2017Article
- The non-canonical NF-κB pathway in immunity and inflammation.Nature reviews. Immunology · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Th17 cells play an important role in mediating autoimmune diseases, but the molecular mechanism underlying Th17 differentiation is incompletely understood. We show here that NF-kappaB-inducing kinase (NIK), which is known to regulate B-cell maturation and lymphoid organogenesis, is important for the induction of Th17 cells. NIK-deficient naive CD4 T cells are attenuated in the differentiation to Th17 cells, although they are competent in committing to the other effector lineages. Consistently, NIK knockout mice are resistant to experimental autoimmune encephalomyelitis, a disease model that involves the function of Th17 cells. This phenotype was also detected in Rag2 knockout mice reconstituted with NIK-deficient T cells, confirming a T-cell intrinsic defect. We further show that NIK mediates synergistic activation of STAT3 by T-cell receptor and IL-6 receptor signals. NIK deficiency attenuates activation of STAT3 and induction of STAT3 target genes involved in Th17-commitment program. These findings establish NIK as an important signaling factor that regulates Th17 differentiation and experimental autoimmune encephalitis induction.
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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.