ArticleFrontiers in immunology2018
Interleukin-6 and Type-I Collagen Production by Systemic Sclerosis Fibroblasts Are Differentially Regulated by Interleukin-17A in the Presence of Transforming Growth Factor-Beta 1.
Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.
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Who cites it
44 citing papers in PubMed, 1 synthesis or guideline pooled it, 66 citations in OpenAlex.
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- Loading of therapeutic cell penetrating peptides into extracellular vesicles for pulmonary fibrosis.Journal of controlled release : official journal of the Controlled Release Society · 2026Article
- Unveiling the choroidal immune landscape revealed interferon-gamma and TNF-alpha as novel therapeutic targets in dry AMD.Science China. Life sciences · 2026Article
- Immunopathological mechanisms and targeted intervention strategies for chronic chikungunya arthritis: from viral persistence to autoimmunity.Frontiers in immunology · 2026Review
- Comparison of the Transcriptomic Signatures of Skin and Lung Fibroblasts from Patients with Systemic Sclerosis.Fibrosis (Hong Kong, China) · 2026Article
- Article
- Comparative efficacy of fractional CO₂ laser combined with concentrated growth factor (CGF) for treating hypertrophic scars in rabbit ears.Lasers in medical science · 2025Article
- Human tissue kallikrein 14 induces the expression of IL-6, IL-8, and CXCL1 in skin fibroblasts through protease-activated receptor 1 signaling.The FEBS journal · 2025Article
- LangerinClinical, cosmetic and investigational dermatology · 2025Review
- Vimentin immunization induces TH2/TH17 cell activation and autoantibody production in a novel mouse model of bleomycin induced systemic sclerosis.Frontiers in immunology · 2025Article
- Staphylococcus aureus adapts to exploit collagen-derived proline during chronic infection.Nature microbiology · 2024Article
- Effector and regulatory B-cell imbalance in systemic sclerosis: cooperation or competition?Clinical rheumatology · 2024Review
- The Role of TLR7 and TLR9 in the Pathogenesis of Systemic Sclerosis.International journal of molecular sciences · 2024Article
- Navigating the Cytokine Seas: Targeting Cytokine Signaling Pathways in Cancer Therapy.International journal of molecular sciences · 2024Review
- The Communication from Immune Cells to the Fibroblasts in Keloids: Implications for Immunotherapy.International journal of molecular sciences · 2023Review
- Protein-Bound Uremic Toxins in Senescence and Kidney Fibrosis.Biomedicines · 2023Review
- Collagen Fibril Orientation Instructs Fibroblast Differentiation Via Cell Contractility.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Fibroblasts are not just fibroblasts: clear differences between dermal and pulmonary fibroblasts' response to fibrotic growth factors.Scientific reports · 2023Article
- Umbilical-Cord-Derived Mesenchymal Stromal Cells Modulate 26 Out of 41 T Cell Subsets from Systemic Sclerosis Patients.Biomedicines · 2023Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Functional cytokine networks have been poorly characterized in systemic sclerosis (SSc). While interleukin-17A (IL-17A) is increased in SSc skin and other organs, its role is still debated, particularly considering fibrogenesis. We uncover here a dual function of IL-17A in the presence of transforming growth factor-β 1 (TGF-β), the master pro-fibrotic cytokine. In the one hand, we report an unexpected synergic activity resulting in enhanced production of IL-6 by dermal fibroblasts; in the other hand, a substantial inhibition of type I collagen (col-I) production. IL-17A or TGF-β enhanced the production of IL-6 by 8- to 16-folds when compared to control in healthy donors (HD) and SSc cultures. However, the joint presence of IL-17A and TGF-β resulted in robustly exuberant responses with levels of IL-6 up to 100-folds higher than those observed in untreated cells. Inhibition of NFκB signaling pathway preferentially inhibited the production of IL-6 driven by IL-17A in HD fibroblasts, while inhibition of PI3K preferentially inhibited the production of IL-6 driven by TGF-β. Interestingly, when p38 MAPK was inhibited, substantial reduction of IL-6 production was observed for both IL-17A and TGF-β. Consistently with the inhibition experiments, the combined stimulation of fibroblasts by IL-17A and TGF-β resulted in 1.8-fold increase in p38 MAPK phosphorylation (
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