IL-18 can induce interferon (IFN)-γ in the presence of IL-12. Because IL-18 appears to be essential for IFN-γ production, it plays a role in regulating IFN-γ production. IL-18 acts on Th1 cells, nonpolarized T cells, natural killer (NK) cells, B cells, and dendritic cells to produce IFN-γ in the presence of IL-12. IL-18 acts as a bridge to link the innate immune response to IFN-γ production by driving T-helper (Th) 1 polarization and priming NK cells, both resulting in high level production of IFN-γ. IL-18 harbors the unique property of inducing Fas ligand expression on NK cells, facilitating their killing of infected cells by Fas-mediated apoptosis.
In addition to its potent induction of IFN-γ, IL-18 activates CD8+T cells, which plays a central role in viral clearance. Viral infections promote the production of various proinflammatory cytokines which can augment CD8 T cells. This includes type I interferons (IFN), interleukin-12 family members, IL-6, and related cytokines, as well as IL-1 family members including IL-18 and IL-33. The relative abundance and kinetics of expression of these factors depend upon the properties of the infecting pathogen, but they all impact the ensuing CD8 T cell response.
You may want to refer to the articles attached below.
Article Anti-viral CD8 T cells and the cytokines that they love
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