IFNG and rheumatoid arthritis: Extrapolating our murine primary and human RA studies we infer that the pathogenic and inflammatory Th17 cells are the IL-17A+ (Th17) and dual IFN-γ+/IL-17A+ (Th1/Th17) cells that might persist due to their inherent AICD insensitivity and contribute to the episodic inflammation [42].