ArticleNature communications2015
Proinflammatory TLR signalling is regulated by a TRAF2-dependent proteolysis mechanism in macrophages.
Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
65 citing papers in PubMed, 1 synthesis or guideline pooled it, 93 citations in OpenAlex.
- Transcriptome-Wide Association Study for Inflammatory Bowel Disease Reveals Novel Candidate Susceptibility Genes in Specific Colon Subsites and Tissue Categories.Journal of Crohn's & colitis · 2022Pooled it
- MK2/p38/p53 Suppress Basal IL-1β and Non-Canonical NF-κB Signaling in Macrophages.International journal of molecular sciences · 2026Article
- Indigestible carbohydrates suppress colorectal cancer through IRF6/TRAF3/IFNα pathway.Discover oncology · 2026Article
- Inflammatory bowel disease in a young female patient with a novel de novo TRAF3 frameshift variant responsive to ustekinumab: a case report.Intestinal research · 2026Article
- Ubiquitin-Modifying Enzymes as Cell-Fate Regulators in Intestinal Inflammation.International journal of biological sciences · 2026Review
- Adaptor proteins regulating tumor-associated macrophage polarization during cancer progression.Oncoscience · 2026Review
- Inflammation and cancer cell survival: TRAF2 as a key player.Cell death & disease · 2025Review
- Article
- Comparative Evaluation of the Chemical Components and Anti-Inflammatory Potential of Yellow- and Blue-FloweredMetabolites · 2024Article
- Targeting Macrophage Polarization for Reinstating Homeostasis following Tissue Damage.International journal of molecular sciences · 2024Review
- A Novel Cargo Delivery System-AnCar-ExoAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- The natural compound Sanggenon C inhibits PRRSV infection by regulating the TRAF2/NF-κB signalling pathway.Veterinary research · 2023Article
- Macrophage RIPK3 triggers inflammation and cell death via the XBP1-Foxo1 axis in liver ischaemia-reperfusion injury.JHEP reports : innovation in hepatology · 2023Article
- TRAF3/STAT6 axis regulates macrophage polarization and tumor progression.Cell death and differentiation · 2023Article
- TRAF2 promotes M2-polarized tumor-associated macrophage infiltration, angiogenesis and cancer progression by inhibiting autophagy in clear cell renal cell carcinoma.Journal of experimental & clinical cancer research : CR · 2023Article
- The adaptor protein TRAF3 is an immune checkpoint that inhibits myeloid-derived suppressor cell expansion.Frontiers in immunology · 2023Article
- Review
- Cellular inhibitor of apoptosis 2 (cIAP2) restricts neuroinflammation during experimental autoimmune encephalomyelitis.Journal of neuroinflammation · 2022Article
- Immune Cell Plasticity in Inflammation: Insights into Description and Regulation of Immune Cell Phenotypes.Cells · 2022Review
- SGK1 negatively regulates inflammatory immune responses and protects against alveolar bone loss through modulation of TRAF3 activity.The Journal of biological chemistry · 2022Article
5 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Signal transduction from toll-like receptors (TLRs) is important for innate immunity against infections, but deregulated TLR signalling contributes to inflammatory disorders. Here we show that myeloid cell-specific ablation of TRAF2 greatly promotes TLR-stimulated proinflammatory cytokine expression in macrophages and exacerbates colitis in an animal model of inflammatory bowel disease. TRAF2 deficiency does not enhance upstream signalling events, but it causes accumulation of two transcription factors, c-Rel and IRF5, known to mediate proinflammatory cytokine induction. Interestingly, TRAF2 controls the fate of c-Rel and IRF5 via a proteasome-dependent mechanism that also requires TRAF3 and the E3 ubiquitin ligase cIAP. We further show that TRAF2 also regulates inflammatory cytokine production in tumour-associated macrophages and facilitates tumour growth. These findings demonstrate an unexpected anti-inflammatory function of TRAF2 and suggest a proteasome-dependent mechanism that limits the proinflammatory TLR signalling.
Indexed as
Identifiers
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.