Involvement of Tumor Necrosis Factor Receptor Type II in FoxP3 Stability and as a Marker of Treg Cells Specifically Expanded by Anti-Tumor Necrosis Factor Treatments in Rheumatoid Arthritis.

François SantinonMaxime BatignesMajda Lyna MebrekJerôme BitonGaëlle ClavelRoxane HervéDelphine LemeiterMagali BrecklerFlorence BusatoJorg TostMarianne ZiolMarie-Christophe BoissierPatrice DeckerLuca SemeranoNatacha Bessis

Published in: Arthritis & rheumatology (Hoboken, N.J.) (2020)

TNFRII expression identifies a subset of Treg cells that are characterized by stable expression of Foxp3 via gene hypomethylation, and adoptive transfer of TNFRII-expressing Treg cells ameliorates inflammation in experimental models. Expansion and activation of TNFRII+ Treg cells may be one of the mechanisms by which anti-TNF agents control inflammation in RA, but not in SpA.

Keyphrases

rheumatoid arthritis
induced apoptosis
cell cycle arrest
oxidative stress
poor prognosis
cell death
bone marrow
genome wide identification