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. Author manuscript; available in PMC: 2020 Apr 16.
Published in final edited form as: Nat Rev Immunol. 2015 Feb 1;15(2):87–103. doi: 10.1038/nri3787

Figure 3. Positive and negative effects of type I interferons during bacterial infection.

Figure 3

Low level autocrine IFNα/β signalling primes the production of interleukin-10 (IL-10), pro-inflammatory cytokines and antimicrobial effector mechanisms. 2b: type I IFN induces IL-1Rα, which in turn inhibits IL-1 signaling. IL-10 mediates a negative feedback loop, suppressing production of pro-inflammatory cytokines including IL-12, TNFα and IL-1α/β. Upon infection high levels of IFNα/β affecting myeloid cells can be contributed by autocrine production as well as from exocrine cellular sources. IFNα/β can also suppress pro-inflammatory cytokine production in an IL-10 independent manner. A major suppressive mechanism of type I IFN is down-regulation of the IFNγR, thus abrogating IFNγ dependent host protective immune responses. IFNα/β signalling can promote high levels of IL-10 production as well as the induction of pro-apoptotic factors. IL-1α/β induces COX-2 dependent PGE2. PGE2 and IL-1 inhibit type I IFN expression and downstream effects