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Joint Bone Spine
Volume 79, n° 2
pages 119-123 (mars 2012)
Doi : 10.1016/j.jbspin.2011.09.017
accepted : 28 September 2011
TNF⍺: Activator or inhibitor of regulatory T cells?
 

Jérôme Biton a, Marie-Christophe Boissier a, b, Natacha Bessis a,
a EA4222, Li2P, Sorbonne Paris-Cité, université Paris-13, 74, rue Marcel-Cachin, 93000 Bobigny, France 
b Service de rhumatologie, hôpital Avicenne, AP–HP, 125, rue de Stalingrad, 93000 Bobigny, France 

Corresponding author. Tel.: +33 1 48 38 73 02; fax: +33 1 48 38 88 93.
Abstract

TNF⍺ is a cytokine that is central to the pathogenesis of several autoimmune diseases. More specifically, the deleterious effects of TNF⍺ in rheumatoid arthritis (RA) are well established. The proinflammatory influence of TNF⍺ in RA is related both to direct effects mediated by the induction of other proinflammatory cytokines, metalloproteinases, and free radicals; and to modulation of the regulatory T cells (Tregs). Furthermore, the TNF⍺ antagonists used to treat RA can induce the emergence of a distinctive Treg subpopulation. Nevertheless, a recent body of data suggests that TNF⍺ may also exert anti-inflammatory effects, which may be mediated in part via Tregs. TNF⍺ binds to the TNF receptor 2 expressed preferentially at the Treg surface, thereby activating and promoting the development of Tregs. Data from patients with RA and more recent evidence obtained in the absence of disease are consistent with a paradoxical effect of TNF⍺ on Tregs. TNF⍺ may have different effects on naturally occurring Tregs and induced Tregs.

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Keywords : TNF⍺ regulatory T cells, TNF⍺ antagonists, Rheumatoid arthritis




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