TBK1 and infection: The complement anaphylatoxins, C5a and C3a that are generated during activation of the complement cascade in response to infection are shown to inhibit the production of detrimental IFN-β by damping the expression of DEAD-box helicase 41 (DDX41), STING, phosphorylated TBK1, and phosphorylated p38 mitogen-activated protein kinase (MAPK), which play critical roles in the type I IFN induction upon L. monocytogenes infection (233).