FOXP3 and rheumatoid arthritis: FoxP3+ Tregs sampled from the SF of RA patients are able to suppress the proliferation of effector T cells [31], but Ehrenstein et al. reported that, while Tregs from RA patients do suppress proliferation, they are defective in their ability to suppress pro-inflammatory cytokine production [34], and thus this process is not regulated, resulting in inflammation.