This suggests that CD73 expression on Th17 cells could contribute in RA to limit the aggressiveness of the disease through the generation of Ado that could impair their own expansion but not IL-17A production as we previously demonstrated the inability of Ado to alter IL-17A secretion in contrast to other cytokines (IFN-γ, GM-CSF, IL-22, IL-10, IL-13) [12,30]. This evidence concerns the gene IFNG and rheumatoid arthritis.