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. 2015 Jun 16;6:303. doi: 10.3389/fimmu.2015.00303

Figure 1.

Figure 1

Proposed mechanisms of MAIT cell activation in infection and sterile disease. Bacteria or yeast (1) can stimulate MAIT cell activation following infection or phagocytosis by antigen presenting cells. These cells can then present microbial-derived vitamin B metabolites via MR1 (associated with β2-microglobulin) to the Vα7.2-bearing MAIT TCR. Upon infection, antigen presenting cells also produce IL-12 and IL-18 cytokines that can activate MAIT cells in an antigen-independent mechanism. The production of IL-7 from hepatocytes can act synergistically to enhance MAIT cell activation. Viruses (2) can stimulate MAIT cells through detection of their molecular patterns by pattern recognition receptors, such as ssRNA by TLR8 on antigen presenting cells, resulting in the production of IL-12 and IL-18. In sterile disease (3), such as autoimmunity, cells that pathologically express cytokines IL-12 and IL-18 can activate MAIT cells. The activation of MAIT cells (4) results in the production of Th1 cytokines IFNγ and TNFα, Th17 cytokines IL-17 and IL-22 (particularly by small intestine-derived MAIT cells), and release of perforin and granzyme B to directly kill infected cells.