Th1.17 compose a recently described subset of highly polyfunctional and thus potentially more harmful CD4+ effector T cells (Teff) than classical Th17 as they co-produce interferon-γ (IFN-γ) and interleukin-17A (IL-17A). For this reason, Th1.17 rise increasing interest in RA and PsA since they seem involved in their pathophysiology. Hyper activation of Teff in RA and PsA results partly from a deficiency in regulatory mechanisms of Teff's pro-inflammatory functions. The ecto-nucleotidase CD73 delineates Teff enriched in Th1.17 features and acts as a regulatory mechanism for these pro-inflammatory cells. Considering that MTX, usually used as first line treatment of RA and PsA, increases extracellular concentrations of adenosine monophasphate (AMP) and immunosuppressive adenosine, the investigators hypothesized that CD4+CD73+ T cell effector population enriched in Th1.17 and Th17 cells may participate in the pathogenicity of RA and PsA but also in the resistance to MTX treatment through the specific expression of CD73 essential for Ado generation and which is down-regulated on proliferating T cells.
