Does Etanercept Influence Tweak Modulation of Inflammation During Inflammatory Rheumatisms (Psoriatic Arthritis and Rheumatoid Arthritis)?
NCT02164214 · Status: COMPLETED · Phase: PHASE3 · Type: INTERVENTIONAL · Enrollment: 60
Last updated 2015-09-10
Summary
TWEAK (TNF weakly inducer of apoptosis) is a type II-transmembrane protein, member of the TNF ligand superfamily that can be cleaved to function as a soluble cytokine. Depending on target cell type, TWEAK triggers multiple cellular responses ranging from modulation of inflammation to cell death when it binds to its main receptor, Fn 14. Our team has been the first to describe pro-inflammatory effects of TWEAK during central nervous system inflammation. Various data support the possibility that TWEAK produced by synovial macrophages may contribute to chronic synovitis in animal models and in humans. In psoriatic arthritis (PsoA), anti-TNF therapy has been successful concording with the key role of TNF in the pathogenesis of this disease and the generation by psoriatic patients of neutralizing anti-TNF autoantibodies referred as "beneficial autoimmunity to pro-inflammatory mediators". In 2010, Van Kuijk et al. have described a high expression of TWEAK in the inflammatory synovial of PsoA and rheumatoid arthritis (RA) patients before and after anti-TNF therapy. The role of TNF-alpha in the regulation of TWEAK expression remains unclear.
Conditions
- Inflammatory Rheumatism
- Psoriatic Arthritis
- Rheumatoid Arthritis
Interventions
- DRUG
-
etanercept Treatment
Sponsors & Collaborators
-
Assistance Publique Hopitaux De Marseille
lead OTHER
Principal Investigators
-
LOIC MONDOLONI · Assistance Publique Hopitaux De Marseille
Study Design
- Allocation
- NON_RANDOMIZED
- Purpose
- TREATMENT
- Masking
- NONE
- Model
- PARALLEL
Eligibility
- Min Age
- 18 Years
- Sex
- ALL
- Healthy Volunteers
- No
Timeline & Regulatory
- Start
- 2011-09-30
- Primary Completion
- 2015-03-31
- Completion
- 2015-09-30
Countries
- France
Study Locations
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