Santinon F, Batignes M, Mebrek ML, et al. - In order to examine the involvement of Treg cells expressing tumor necrosis factor receptor type II (TNFRII) in exerting control of inflammation in experimental models and in the response to anti-TNF treatments in patients with rheumatoid arthritis (RA) or spondyloarthritis (SpA), researchers explored the role of TNFRII in Treg cells applying a multilevel translational approach. This study assessed Treg cell stability by examining the methylation status of the FoxP3 locus using bisulfite sequencing. The evolution of the TNFRII+ Treg cell population before and after targeted treatment was monitored in individuals with RA and those with SpA. The outcomes indicated that TNFRII expression distinguishes a subset of Treg cells that are marked by stable expression of FoxP3 via gene hypomethylation, and adoptive transfer of TNFRII-expressing Treg cells ameliorates inflammation in experimental models. It was demonstrated that 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.