ArticleJCI insight2018
TNF and granulocyte macrophage-colony stimulating factor interdependence mediates inflammation via CCL17.
Article in JCI insight, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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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.
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Who cites it
37 citing papers in PubMed, 56 citations in OpenAlex.
- Randomized, placebo-controlled study on the effects of intravenous GSK3858279 (anti-CCL17) on a battery of evoked pain tests in healthy participants.Clinical and translational science · 2024Trial
- JMJD3-driven epigenetic reprogramming of p16Bone research · 2026Article
- Innate lymphoid cells in rheumatoid arthritis as mediators of pathology and resolution.Nature reviews. Rheumatology · 2026Review
- Differences in Itch Quality Between Interleukin-31 and Thymus and Activation-Regulated Chemokine of Japanese Atopic Dermatitis.Mayo Clinic proceedings. Innovations, quality & outcomes · 2026Article
- Tofacitinib repairs inflammation and mitochondrial dysregulation in GM-CSF-reprogrammed RA macrophages.Cellular & molecular immunology · 2026Article
- Pathogenic GM-CSF drives functional diversification of inflammatory macrophages in autoimmune arthritis.Science advances · 2026Article
- hsa_circ_0006168 drives microglial activation in TNC via miR-99b-5p/KDM6B axis to promote central sensitization in migraine.The journal of headache and pain · 2026Article
- The CCL17/CCL22-CCR4 Axis in Pain Pathogenesis: A Comprehensive Review of Immune-Mediated Mechanisms and Therapeutic Opportunities.Molecular neurobiology · 2025Review
- Screening of the FDA-approved drug library identifies CCL17 inhibitors that block arthritic pain.Scientific reports · 2025Article
- Therapeutic blockade of CCL17 in obesity-exacerbated osteoarthritic pain and disease.PloS one · 2025Article
- Self-Assembled Carrier Free Oligomeric Proanthocyanidin/Tetrandrine Nanoparticles Ameliorate Osteoarthritis via Anti-Inflammatory and Anti-Ferroptotic Pathways.International journal of nanomedicine · 2025Article
- Inflammation induced by the new lineage ofFrontiers in immunology · 2025Article
- Emerging role of Jumonji domain-containing protein D3 in inflammatory diseases.Journal of pharmaceutical analysis · 2024Review
- Can serum granulocyte-macrophage colony-stimulating factor and CCL17 levels be a marker of disease activation in spondyloarthritis?Archives of rheumatology · 2024Article
- The mode of action of IL-23 in experimental inflammatory arthritic pain and disease.Arthritis research & therapy · 2024Article
- Epigenetic and transcriptional regulation of CCL17 production by glucocorticoids in arthritis.iScience · 2023Article
- TRAIL promotes the polarization of human macrophages toward a proinflammatory M1 phenotype and is associated with increased survival in cancer patients with high tumor macrophage content.Frontiers in immunology · 2023Article
- The role of interleukin (IL)-23 in regulating pain in arthritis.Arthritis research & therapy · 2022Article
- Immunity and pain in the eye: focus on the ocular surface.Clinical and experimental immunology · 2022Review
- Effects of swimming training on myocardial protection in rats.Biomedical reports · 2022Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
TNF and granulocyte macrophage-colony stimulating factor (GM-CSF) have proinflammatory activity and both contribute, for example, to rheumatoid arthritis pathogenesis. We previously identified a new GM-CSF→JMJD3 demethylase→interferon regulatory factor 4 (IRF4)→CCL17 pathway that is active in monocytes/macrophages in vitro and important for inflammatory pain, as well as for arthritic pain and disease. Here we provide evidence for a nexus between TNF and this pathway, and for TNF and GM-CSF interdependency. We report that the initiation of zymosan-induced inflammatory pain and zymosan-induced arthritic pain and disease are TNF dependent. Once arthritic pain and disease are established, blockade of GM-CSF or CCL17, but not of TNF, is still able to ameliorate them. TNF is required for GM-CSF-driven inflammatory pain and for initiation of GM-CSF-driven arthritic pain and disease, but not once they are established. TNF-driven inflammatory pain and TNF-driven arthritic pain and disease are dependent on GM-CSF and mechanistically require the same downstream pathway involving GM-CSF→CCL17 formation via JMJD3-regulated IRF4 production, indicating that GM-CSF and CCL17 can mediate some of the proinflammatory and algesic actions of TNF. Given we found that TNF appears important only early in arthritic pain and disease progression, targeting a downstream mediator, such as CCL17, which appears to act throughout the course of disease, could be effective at ameliorating chronic inflammatory conditions where TNF is implicated.
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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.