Altogether, the above findings indicate that: i) MAIT cells constitutively express high levels of IL-12R and IL-18R and are thus poised to respond to these cytokines during infection with SAg-producing bacteria; ii) the cytokine-mediated pathway of MAIT cell activation is dominant over the iTCR-dependent pathway during exposure to SAgs; iii) and this pathway is driven by IL-18 and IL-12 but not by IFN-γ at the outset. Here, IL12RB1 is linked to infection.