IL-17 increased the production of vascular endothelial growth factor in rheumatoid arthritis synoviocytes

Ryu, Sun Suk; Lee, J. H.; Kim, S. I.

doi:10.1007/s10067-005-1081-1

Cited by 81 publications

(56 citation statements)

References 35 publications

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“…Deviating Th1 responses into Th2 responses improved Th1 cellmediated inflammation and protected against inflammation-induced angiogenesis in mice and humans (36)(37)(38). Most importantly, Th1 cells seem to coevolve simultaneously with IL-17-producing Th17 cells (39); IL-17 is a cytokine with strong proangiogenic effects (40,41). Because Th1 cell-associated skin and joint inflammation are associated with both Th17 cells and mast cells, the relative contribution of mast cells to inflammation-induced angiogenesis remains to be determined.…”

Section: Discussionmentioning

confidence: 99%

Targeted mast cell silencing protects against joint destruction and angiogenesis in experimental arthritis in mice

Kneilling

Hültner

Pichler

et al. 2007

Arthritis & Rheumatism

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Objective. Induction of arthritis with autoantibodies against glucose-6-phosphate isomerase (GPI) is entirely independent of T cells and B cells but isResults. Comparing wild-type mice, mast celldeficient Kit W /Kit W-v mice, and mast cell-reconstituted Kit W /Kit W-v mice, we first showed that intraarticular and intraperitoneal mast cell engraftment fully restores susceptibility to antibody-induced arthritis, angiogenesis, and ␣v␤3 integrin activation. Importantly, selective mast cell silencing with either salbutamol or cromolyn prevented ␣v␤3 integrin activation, angiogenesis, and joint destruction.Conclusion. Mast cell engraftment fully restores susceptibility to ␣v␤3 integrin activation, angiogenesis, and joint destruction in GPI antibody-induced arthritis. Importantly, selective mast cell stabilization prevents ␣v␤3 integrin activation, angiogenesis, and joint destruction.

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Section: Discussionmentioning

confidence: 99%

Targeted mast cell silencing protects against joint destruction and angiogenesis in experimental arthritis in mice

Kneilling

Hültner

Pichler

et al. 2007

Arthritis & Rheumatism

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“…Of note, IL-17 was shown to be proangiogenic and to induce endothelial cell invasion (10). IL-17 has the potential to upregulate VEGF from RA synoviocytes (11) and to promote the development of microvessel structures in RA, as well as in tumor growth (12,13). Recently, a subset of effector Th cells, the IL-17-producing T cell (Th17), was implicated in the pathogenesis of various autoimmune diseases, including uveitis, arthritis, multiple sclerosis, psoriasis, and inflammatory bowel disease.…”

mentioning

confidence: 99%

IL-23–Independent Induction of IL-17 from γδT Cells and Innate Lymphoid Cells Promotes Experimental Intraocular Neovascularization

Hasegawa

Sonoda

Shichita

et al. 2013

The Journal of Immunology

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Choroidal neovascularization (CNV) is a characteristic of age-related macular degeneration. Genome-wide association studies have provided evidence that the immune system is involved in the pathogenesis of age-related macular degeneration; however, the role of inflammatory cytokines in CNV has not been established. In this study, we demonstrated that IL-17 had a strong potential for promoting neovascularization in a vascular endothelial growth factor–independent manner in laser-induced experimental CNV in mice. Infiltrated γδT cells and Thy-1+ innate lymphoid cells, but not Th17 cells, were the main sources of IL-17 in injured eyes. IL-23 was dispensable for IL-17 induction in the eye. Instead, we found that IL-1β and high-mobility group box 1 strongly promoted IL-17 expression by γδT cells. Suppression of IL-1β and high-mobility group box 1, as well as depletion of γδT cells, reduced IL-17 levels and ameliorated experimental CNV. Our findings suggest the existence of a novel inflammatory cytokine network that promotes neovascularization in the eye.

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“…These cytokines regulate the inflammatory response and activities related to joint destruction, thereby participating in RA pathogenesis. 33,34) We observed that SD, a non-steroidal anti-inflammatory agent, improved the inflammation parameters analysed. These results are similar to those observed for OLM.…”

Section: Discussionmentioning

confidence: 77%

Olmesartan Prevented Intra-articular Inflammation Induced by Zymosan in Rats

Guerra

Menezes

Araújo

et al. 2016

Biological & Pharmaceutical Bulletin

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The objective of this study was to study the effect of olmesartan medoxomil (OLM), an antihypertensive drug, on intra-articular inflammation induced by zymosan (Zy) in Wistar rats. Intra-articular inflammation was induced in the right knees of rats by 1 mg Zy dissolved in saline. The animals were divided into the following groups: saline only (oral saline and intra-articular saline); Zy only (intra-articular Zy and oral saline), and intra-articular Zy and oral OLM (5, 15, or 30 mg/kg) or diclofenac sodium (SD; 100 mg/ kg). Twenty-four hours after Zy injection, synovial fluid was collected for total leukocyte counts, blood was collected for biochemical measurements, and synovial tissue was collected for histopathology, immunohistochemistry, immunofluorescence and myeloperoxidase (MPO), malonaldehyde (MDA), and non-protein sulphydryl (NPSH) assays. OLM doses of 15 and 30 mg/kg had protective effects, as evidenced by improved histopathological parameters of synovium, reduced total leukocyte counts, reduced MPO and MDA levels, and increased NPSH group levels compared with the Zy group. OLM reduced immunostaining for cyclooxygenase 2, tumour necrosis factor and interleukin 17 and increased immunostaining for superoxide dismutase and glutathione peroxidase. SD produced similar results. The drugs studied caused no change in biochemical parameters of the animals. OLM showed protective effects in this model of Zy-induced intra-articular inflammation.

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IL-17 increased the production of vascular endothelial growth factor in rheumatoid arthritis synoviocytes

Cited by 81 publications

References 35 publications

Targeted mast cell silencing protects against joint destruction and angiogenesis in experimental arthritis in mice

Targeted mast cell silencing protects against joint destruction and angiogenesis in experimental arthritis in mice

IL-23–Independent Induction of IL-17 from γδT Cells and Innate Lymphoid Cells Promotes Experimental Intraocular Neovascularization

Olmesartan Prevented Intra-articular Inflammation Induced by Zymosan in Rats

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