Abstract
Type I and III interferons (IFNs) are archetypally antiviral cytokines that are induced in response to recognition of foreign material by pattern recognition receptors (PRRs). Though their roles in anti-viral immunity are well established, recent evidence suggests that they are also crucial mediators of inflammatory processes during bacterial infections. Type I and III IFNs restrict bacterial infection in vitro and in some in vivo contexts. IFNs mainly function through the induction of hundreds of IFN-stimulated genes (ISGs). These include PRRs and regulators of antimicrobial signaling pathways. Other ISGs directly restrict bacterial invasion or multiplication within host cells. As they regulate a diverse range of anti-bacterial host responses, IFNs are an attractive virulence target for bacterial pathogens. This review will discuss the current understanding of the bacterial effectors that manipulate the different stages of the host IFN response: IFN induction, downstream signaling pathways, and target ISGs.
Highlights
The first interferons (IFNs) were discovered in 1957 by Alick Isaacs and Jean Lindenmann when they noticed that tissues inoculated with inactivated virus produced a soluble substance that “interfered” with subsequent viral infection (Isaacs and Lindenmann, 1957)
Over 20 years before Charles Janeway’s (Janeway, 1989) predictions on pattern recognition, Isaacs and Lindenmann had recognized the fundamental properties of IFN: a cytokine produced in response to detection of pathogen associated molecular patterns (PAMPs) by pattern recognition receptors (PRRs), that can protect tissues from subsequent microbial infections
There are three families of IFN: type I, II, and III, which bind to the IFNa receptor (IFNAR), IFNg receptor (IFNGR) and IFNl receptor (IFNLR), respectively
Summary
The first interferons (IFNs) were discovered in 1957 by Alick Isaacs and Jean Lindenmann when they noticed that tissues inoculated with inactivated virus produced a soluble substance that “interfered” with subsequent viral infection (Isaacs and Lindenmann, 1957). TARGETING OF TYPES I AND III INTERFERON EXPRESSION BY BACTERIAL EFFECTORS In order to control their host, pathogenic bacteria secrete effectors that manipulate different stages of the IFN response, from its production to signaling and even ISG functions.
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