Our indications were supported by the fact that miR-155 overexpression in activated T cells promotes autoimmune inflammation through enhancing T cell activation and proliferation, production and release of pro-inflammatory cytokines, polarization of Th cells into IFN-γ-secreting Th1 and IL-17-secreting Th17 phenotypes, and induction of macrophage inflammatory responses (20, 21, 45), mechanisms that are related to GCA pathogenesis (4, 6, 8). The gene discussed is IL17A; the disease is temporal arteritis.