Assistance Publique Hopitaux de Marseille
Marseille, 13354, France
NCT Number: NCT02164214
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.
Looking for future studies?
Notify Me18 year and older
All sexes
Interventional
Phase 3
Marseille, 13354, France
Healthy volunteers accepted: No
Only the study team can determine whether someone qualifies for participation.
Inclusion criteria
· Group PR
Exclusion criteria
Time frame: 42 months
samples blood before and after etanercept Treatment
Assistance Publique Hopitaux De Marseille
Other
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