ArticleClinical and experimental immunology2000
IL-17 regulates gene expression and protein synthesis of the complement system, C3 and factor B, in skin fibroblasts.
Article in Clinical and experimental immunology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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.
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Who cites it
15 citing papers in PubMed, 55 citations in OpenAlex.
- Tocotrienol suppresses colitis-associated cancer progression through TLR4 signaling in a mouse model of colorectal cancer.Current research in toxicology · 2024Article
- The Yin and Yang of IL-17 in Systemic Sclerosis.Frontiers in immunology · 2022Review
- Article
- Complement activation links inflammation to dental tissue regeneration.Clinical oral investigations · 2020Review
- Characterization of the interleukin-17 effect on articular cartilage in a translational model: an explorative study.BMC rheumatology · 2020Article
- IL-17A deficiency mitigates bleomycin-induced complement activation during lung fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
- Biomarkers of systemic inflammation in farmers with musculoskeletal disorders; a plasma proteomic study.BMC musculoskeletal disorders · 2016Article
- Inflammaging in skin and other tissues - the roles of complement system and macrophage.Inflammation & allergy drug targets · 2014Review
- A cytokine-centric view of the pathogenesis and treatment of autoimmune arthritis.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2011Review
- Interleukin-17 synergizes with IFNγ or TNFα to promote inflammatory mediator release and intercellular adhesion molecule-1 (ICAM-1) expression in human intervertebral disc cells.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2011Article
- Complement-mediated regulation of the IL-17A axis is a central genetic determinant of the severity of experimental allergic asthma.Nature immunology · 2010Article
- Breaking old paradigms: Th17 cells in autoimmune arthritis.Clinical immunology (Orlando, Fla.) · 2009Review
- What determines the success or failure of intracellular cutaneous parasites? Lessons learned from leishmaniasis.Medical microbiology and immunology · 2009Review
- The role of T-cell interleukin-17 in conducting destructive arthritis: lessons from animal models.Arthritis research & therapy · 2005Review
- Association of CD4+ CD25+ T cells with prevention of severe destructive arthritis in Borrelia burgdorferi-vaccinated and challenged gamma interferon-deficient mice treated with anti-interleukin-17 antibody.Clinical and diagnostic laboratory immunology · 2004Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human IL-17 is a cytokine secreted by CD4+-activated memory T cells with the profile of effects of a Th1 cytokine. The effects of IL-17 on many cellular constituents of joints suggest that it may participate in inflammatory joint diseases. Proteins of the complement system are known to be regulated by pro- and anti-inflammatory cytokines. The purpose of this work was to study the effect of IL-17 alone and combined with tumour necrosis factor (TNF) on the expression and synthesis of factor B and C3. Fibroblasts were stimulated with the relevant cytokine or cytokines, pulse labelled with 35S-methionine, and the newly synthesized proteins were immunoprecipitated and subjected to SDS-PAGE. Gene expression was determined by Northern blot analysis. IL-17 10 ng/ml induced increases in gene expression and protein synthesis of C3, 2.25 +/- 0.26- and 2.7 +/- 0.7-fold, respectively with concomitant non-significant effects on factor B, 1.5 +/- 0.45- and 2.2 +/- 1. 2-fold, respectively. When both IL-17 and TNF were present simultaneously, the synthesis of factor B increased by 85% more than the expected additive effects of these cytokines separately, while for C3 the effect of both cytokines was 19% lower than the expected additive effect (observed/expected = 0.81). IL-4 reduced the synergistic effect by 50%. We conclude that IL-17 has a regulatory role on C3 expression and synthesis and an amplifying effect on TNF-induced factor B synthesis. Taken together with the evidence that TNF is a major cytokine involved in the inflammation of rheumatoid arthritis, it suggests that IL-17 has a proinflammatory role in the inflammation process of joints. The distinct effects of IL-4, IL-17 and TNF on the synthesis of factor B in fibroblasts suggest that factor B and the alternative pathway of the complement system may play an important role in joint inflammation.
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