ArticleThe Journal of experimental medicine2003
NIK-dependent RelB activation defines a unique signaling pathway for the development of V alpha 14i NKT cells.
Article in The Journal of experimental medicine, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 116 citations in OpenAlex.
- The NF-κB transcription factor RelA directs mucosal-associated invariant T-cell development.Immunology and cell biology · 2026Article
- NF-κB signaling in inflammation and cancer.MedComm · 2021Review
- Thymic development of unconventional T cells: how NKT cells, MAIT cells and γδ T cells emerge.Nature reviews. Immunology · 2020Review
- USP22 controls iNKT immunity through MED1 suppression of histone H2A monoubiquitination.The Journal of experimental medicine · 2020Article
- TRAF3IP3 at the trans-Golgi network regulates NKT2 maturation via the MEK/ERK signaling pathway.Cellular & molecular immunology · 2020Article
- The ins and outs of type I iNKT cell development.Molecular immunology · 2019Review
- Clinical and Immunological Phenotype of Patients With Primary Immunodeficiency Due to Damaging Mutations inFrontiers in immunology · 2019Article
- IAP Antagonists Enhance Cytokine Production from Mouse and Human iNKT Cells.Cancer immunology research · 2018Article
- NF-κB Protects NKT Cells from Tumor Necrosis Factor Receptor 1-induced Death.Scientific reports · 2017Article
- The non-canonical NF-κB pathway in immunity and inflammation.Nature reviews. Immunology · 2017Review
- The Lysine Acetyltransferase GCN5 Is Required for iNKT Cell Development through EGR2 Acetylation.Cell reports · 2017Article
- Id2 Collaborates with Id3 To Suppress Invariant NKT and Innate-like Tumors.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Deficiency of transcription factor RelB perturbs myeloid and DC development by hematopoietic-extrinsic mechanisms.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Dissection of SAP-dependent and SAP-independent SLAM family signaling in NKT cell development and humoral immunity.The Journal of experimental medicine · 2017Article
- Natural Killer T Cells: An Ecological Evolutionary Developmental Biology Perspective.Frontiers in immunology · 2017Review
- Diacylglycerol Kinases in T Cell Tolerance and Effector Function.Frontiers in cell and developmental biology · 2016Review
- Article
- Differential dependence on nuclear factor-κB-inducing kinase among natural killer T-cell subsets in their development.Immunology · 2015Article
- Natural Th17 cells are critically regulated by functional medullary thymic microenvironments.Journal of autoimmunity · 2015Article
- Let-7 microRNAs target the lineage-specific transcription factor PLZF to regulate terminal NKT cell differentiation and effector function.Nature immunology · 2015Article
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Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
Abstract
A defect in RelB, a member of the Rel/nuclear factor (NF)-kappa B family of transcription factors, affects antigen presenting cells and the formation of lymphoid organs, but its role in T lymphocyte differentiation is not well characterized. Here, we show that RelB deficiency in mice leads to a selective decrease of NKT cells. RelB must be expressed in an irradiation-resistant host cell that can be CD1d negative, indicating that the RelB expressing cell does not contribute directly to the positive selection of CD1d-dependent NKT cells. Like RelB-deficient mice, aly/aly mice with a mutation for the NF-kappa B-inducing kinase (NIK), have reduced NKT cell numbers. An analysis of NK1.1 and CD44 expression on NKT cells in the thymus of aly/aly mice reveals a late block in development. In vitro, we show that NIK is necessary for RelB activation upon triggering of surface receptors. This link between NIK and RelB was further demonstrated in vivo by analyzing RelB+/- x aly/+ compound heterozygous mice. After stimulation with alpha-GalCer, an antigen recognized by NKT cells, these compound heterozygotes had reduced responses compared with either RelB+/- or aly/+ mice. These data illustrate the complex interplay between hemopoietic and nonhemopoietic cell types for the development of NKT cells, and they demonstrate the unique requirement of NKT cells for a signaling pathway mediated by NIK activation of RelB in a thymic stromal cell.
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