ArticleJournal of immunology (Baltimore, Md. : 1950)2012
NIK prevents the development of hypereosinophilic syndrome-like disease in mice independent of IKKα activation.
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 24 papers.
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Who cites it
24 citing papers in PubMed, 37 citations in OpenAlex.
- Mouse models of eosinophilic esophagitis: molecular and translational insights.American journal of physiology. Gastrointestinal and liver physiology · 2025Review
- IL-4-STAT6 axis amplifies histamine-induced vascular endothelial dysfunction and hypovolemic shock.The Journal of allergy and clinical immunology · 2024Article
- Not just for lymphoid cells: the role of the noncanonical NF-κB signaling pathway in early and late myelopoiesis with a focus on hypereosinophilic disorders.Journal of leukocyte biology · 2024Review
- Animal models of eosinophilic esophagitis.Journal of leukocyte biology · 2024Review
- NF-κB-Inducing Kinase Governs the Mitochondrial Respiratory Capacity, Differentiation, and Inflammatory Status of Innate Immune Cells.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Delivery of costimulatory blockade to lymph nodes promotes transplant acceptance in mice.The Journal of clinical investigation · 2022Article
- Combined immunodeficiency with autoimmunity caused by a homozygous missense mutation in inhibitor of nuclear factor 𝛋B kinase alpha (IKKα).Science immunology · 2021Article
- Targeting NF-κB-Inducing Kinase (NIK) in Immunity, Inflammation, and Cancer.International journal of molecular sciences · 2020Review
- Nuclear Factor-kappaB in Autoimmunity: Man and Mouse.Frontiers in immunology · 2018Review
- Noncanonical NF-κB signaling and the essential kinase NIK modulate crucial features associated with eosinophilic esophagitis pathogenesis.Disease models & mechanisms · 2017Article
- The ANK repeats of Notch-4/Int3 activate NF-κB canonical pathway in the absence of Rbpj and causes mammary tumorigenesis.Scientific reports · 2017Article
- The non-canonical NF-κB pathway in immunity and inflammation.Nature reviews. Immunology · 2017Review
- Emerging Roles for Noncanonical NF-κB Signaling in the Modulation of Inflammatory Bowel Disease Pathobiology.Inflammatory bowel diseases · 2016Review
- SHARPIN controls the development of regulatory T cells.Immunology · 2016Article
- NIK promotes tissue destruction independently of the alternative NF-κB pathway through TNFR1/RIP1-induced apoptosis.Cell death and differentiation · 2015Article
- Oncogenic activity of BIRC2 and BIRC3 mutants independent of nuclear factor-κB-activating potential.Cancer science · 2015Article
- Targeting signaling factors for degradation, an emerging mechanism for TRAF functions.Immunological reviews · 2015Review
- Carboxyl terminus of HSC70-interacting protein (CHIP) down-regulates NF-κB-inducing kinase (NIK) and suppresses NIK-induced liver injury.The Journal of biological chemistry · 2015Article
- Biallelic loss-of-function mutation in NIK causes a primary immunodeficiency with multifaceted aberrant lymphoid immunity.Nature communications · 2014Article
- Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Immune cell-mediated tissue injury is a common feature of different inflammatory diseases, yet the pathogenetic mechanisms and cell types involved vary significantly. Hypereosinophilic syndrome (HES) represents a group of inflammatory diseases that is characterized by increased numbers of pathogenic eosinophilic granulocytes in the peripheral blood and diverse organs. On the basis of clinical and laboratory findings, various forms of HES have been defined, yet the molecular mechanism and potential signaling pathways that drive eosinophil expansion remain largely unknown. In this study, we show that mice deficient of the serine/threonine-specific protein kinase NF-κB-inducing kinase (NIK) develop a HES-like disease, reflected by progressive blood and tissue eosinophilia, tissue injury, and premature death at around 25-30 wk of age. Similar to the lymphocytic form of HES, CD4(+) T cells from NIK-deficient mice express increased levels of Th2-associated cytokines, and eosinophilia and survival of NIK-deficient mice could be prevented completely by genetic ablation of CD4(+) T cells. Experiments based on bone marrow chimeric mice, however, demonstrated that inflammation in NIK-deficient mice depended on radiation-resistant tissues, implicating that NIK-deficient immune cells mediate inflammation in a nonautonomous manner. Surprisingly, disease development was independent of NIK's known function as an IκB kinase α (IKKα) kinase, because mice carrying a mutation in the activation loop of IKKα, which is phosphorylated by NIK, did not develop inflammatory disease. Our data show that NIK activity in nonhematopoietic cells controls Th2 cell development and prevents eosinophil-driven inflammatory disease, most likely using a signaling pathway that operates independent of the known NIK substrate IKKα.
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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.