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Increased interleukin-17 production in patients with systemic sclerosis
1Chiba University School of Medicine, Chiba City, Japan.
Arthritis and Rheumatism
|November 18, 2000
Summary
Interleukin-17 (IL-17) is overproduced in systemic sclerosis (SSc) patients, particularly in early stages. This cytokine drives SSc pathogenesis by promoting fibroblast proliferation and endothelial cell activation.
Area of Science:
- Immunology
- Rheumatology
Background:
- Systemic sclerosis (SSc) is a complex autoimmune disease characterized by fibrosis.
- The role of T cell-derived cytokines in SSc pathogenesis is not fully understood.
Purpose of the Study:
- To investigate the role of interleukin-17 (IL-17) in the pathogenesis of systemic sclerosis (SSc).
Main Methods:
- IL-17 production was assessed in lymphocytes and serum from SSc patients using RT-PCR and ELISA.
- In vitro studies examined IL-17's effects on fibroblast proliferation and endothelial cell activation.
Main Results:
- IL-17 was overexpressed in T cells and serum of SSc patients, correlating with early disease stages.
- IL-17 stimulated fibroblast proliferation and induced adhesion molecule expression and IL-1 production in endothelial cells.
Conclusions:
- Overproduction of IL-17 by T cells contributes significantly to SSc pathogenesis, especially in early disease.
- IL-17 may drive SSc through fibroblast proliferation and endothelial cell activation, promoting inflammation and fibrosis.