ArticleProceedings of the National Academy of Sciences of the United States of America2012
Transforming growth factor beta-activated kinase 1 (TAK1)-dependent checkpoint in the survival of dendritic cells promotes immune homeostasis and function.
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 39 papers.
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Who cites it
39 citing papers in PubMed, 54 citations in OpenAlex.
- Metabolic and neuroimmune control of rheumatoid arthritis: therapeutic implications of FXR and α7-nAChR axes.Inflammopharmacology · 2026Review
- TAK1 inhibition restores p53 expression and suppresses inflammation and hyperplasia in JIA synovial fibroblasts.Rheumatology (Oxford, England) · 2026Article
- Dendritic Cells: Orchestrators of Immune Responsiveness and Tolerance.Immunological reviews · 2025Review
- Targeting pattern recognition receptors for cancer therapy: Mechanisms and strategies.Acta pharmaceutica Sinica. B · 2025Review
- Neutrophils in cancer: At the crucial crossroads of anti-tumor and pro-tumor.Cancer communications (London, England) · 2025Review
- Emodin Alleviates Monocrotaline-Induced Pulmonary Arterial Hypertension by Directly Targeting TAK1.Drug design, development and therapy · 2025Article
- Precision treatment of viral pneumonia through macrophage-targeted lipid nanoparticle delivery.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- The Innate Immune Microenvironment in Metastatic Breast Cancer.Journal of clinical medicine · 2022Review
- RIG-I-like Receptor Regulation of Immune Cell Function and Therapeutic Implications.Journal of immunology (Baltimore, Md. : 1950) · 2022Review
- Therapeutic potential of paeoniflorin in atherosclerosis: A cellular action and mechanism-based perspective.Frontiers in immunology · 2022Review
- Paeoniflorin attenuates monocrotaline-induced pulmonary arterial hypertension in rats by suppressing TAK1-MAPK/NF-κB pathways.International journal of medical sciences · 2022Article
- Roles of the RANKL-RANK Axis in Immunity-Implications for Pathogenesis and Treatment of Bone Metastasis.Frontiers in immunology · 2022Review
- The scaffold-dependent function of RIPK1 in dendritic cells promotes injury-induced colitis.Mucosal immunology · 2022Article
- Article
- Smad2/4 Signaling Pathway Is Critical for Epidermal Langerhans Cell Repopulation Under Inflammatory Condition but Not Required for Their Homeostasis at Steady State.Frontiers in immunology · 2020Article
- LKB1 orchestrates dendritic cell metabolic quiescence and anti-tumor immunity.Cell research · 2019Article
- Article
- Signaling control of antibody isotype switching.Advances in immunology · 2019Review
- TRAF2 Deficiency in B Cells Impairs CD40-Induced Isotype Switching That Can Be Rescued by Restoring NF-κB1 Activation.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Homeostatic control of dendritic cell (DC) survival is crucial for adaptive immunity, but the molecular mechanism is not well defined. Moreover, how DCs influence immune homeostasis under steady state remains unclear. Combining DC-specific and -inducible deletion systems, we report that transforming growth factor beta-activated kinase 1 (TAK1) is an essential regulator of DC survival and immune system homeostasis and function. Deficiency of TAK1 in CD11c(+) cells induced markedly elevated apoptosis, leading to the depletion of DC populations, especially the CD8(+) and CD103(+) DC subsets in lymphoid and nonlymphoid tissues, respectively. TAK1 also contributed to DC development by promoting the generation of DC precursors. Prosurvival signals from Toll-like receptors, CD40 and receptor activator of nuclear factor-κB (RANK) are integrated by TAK1 in DCs, which in turn mediated activation of downstream NF-κB and AKT-Foxo pathways and established a gene-expression program. TAK1 deficiency in DCs caused a myeloid proliferative disorder characterized by expansion of neutrophils and inflammatory monocytes, disrupted T-cell homeostasis, and prevented effective T-cell priming and generation of regulatory T cells. Moreover, TAK1 signaling in DCs was required to prevent myeloid proliferation even in the absence of lymphocytes, indicating a previously unappreciated regulatory mechanism of DC-mediated control of myeloid cell-dependent inflammation. Therefore, TAK1 orchestrates a prosurvival checkpoint in DCs that affects the homeostasis and function of the immune system.
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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.