ArticleThe Journal of experimental medicine2011
NIK signaling in dendritic cells but not in T cells is required for the development of effector T cells and cell-mediated immune responses.
Article in The Journal of experimental medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 68 citations in OpenAlex.
- Dendritic cell maturation in cancer.Nature reviews. Cancer · 2025Review
- The Ins and Outs of Thymic Epithelial Cell Differentiation and Function.Advances in experimental medicine and biology · 2025Review
- Non-canonical NF-κB signaling limits the tolerogenic β-catenin-Raldh2 axis in gut dendritic cells to exacerbate intestinal pathologies.The EMBO journal · 2024Article
- Role of Ubiquitin Signaling in Modulating Dendritic Cell Function.Advances in experimental medicine and biology · 2024Review
- 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
- NF-κB Inducing Kinase Regulates Intestinal Immunity and Homeostasis.Frontiers in immunology · 2022Review
- 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
- Apigenin Modulates Dendritic Cell Activities and Curbs Inflammation Via RelB Inhibition in the Context of Neuroinflammatory Diseases.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2021Article
- Targeting NF-κB-Inducing Kinase (NIK) in Immunity, Inflammation, and Cancer.International journal of molecular sciences · 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
- CRL4The Journal of experimental medicine · 2018Article
- CD40 Mediates Maturation of Thymic Dendritic Cells Driven by Self-Reactive CD4Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- The non-canonical NF-κB pathway in immunity and inflammation.Nature reviews. Immunology · 2017Review
- 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
- GWAS analysis implicates NF-κB-mediated induction of inflammatory T cells in multiple sclerosis.Genes and immunity · 2016Article
- Cell intrinsic role of NF-κB-inducing kinase in regulating T cell-mediated immune and autoimmune responses.Scientific reports · 2016Article
- NF-κB Pathways in the Pathogenesis of Multiple Sclerosis and the Therapeutic Implications.Frontiers in molecular neuroscience · 2016Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The canonical NF-κB pathway is a driving force for virtually all aspects of inflammation. Conversely, the role of the noncanonical NF-κB pathway and its central mediator NF-κB-inducing kinase (NIK) remains poorly defined. NIK has been proposed to be involved in the formation of T(H)17 cells, and its absence in T(H) cells renders them incapable of inducing autoimmune responses, suggesting a T cell-intrinsic role for NIK. Upon systematic analysis of NIK function in cell-mediated immunity, we found that NIK signaling is dispensable within CD4(+) T cells but played a pivotal role in dendritic cells (DCs). We discovered that NIK signaling is required in DCs to deliver co-stimulatory signals to CD4(+) T cells and that DC-restricted expression of NIK is sufficient to restore T(H)1 and T(H)17 responses as well as cell-mediated immunity in NIK(-/-) mice. When CD4(+) T cells developed in the absence of NIK-sufficient DCs, they were rendered anergic. Reintroduction of NIK into DCs allowed developing NIK(-/-) CD4(+) T cells to become functional effector populations and restored the development of autoimmune disease. Therefore, our data suggest that a population of thymic DCs requires NIK to shape the formation of most αβ CD4(+) T effector lineages during early development.
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