Interferons: Tug of War Between Bacteria and Their Host

Frontiers in Cellular and Infection Microbiology

Charlotte Odendall¹  Ruth E. Dickenson¹  Noémie Alphonse² 

[1] Department of Infectious Diseases, School of Immunology and Microbial Sciences, King’s College London, London, United Kingdom;Department of Infectious Diseases, School of Immunology and Microbial Sciences, King’s College London, London, United Kingdom;Immunoregulation Laboratory, Francis Crick Institute, London, United Kingdom;

关键词: bacterial effectors;    interferons;    interferon-stimulated genes;    janus kinase signal transducer and activator of transcription signaling;    immunity;    microbial pathogenesis;    host-pathogen interactions;   

DOI  :  10.3389/fcimb.2021.624094

来源: Frontiers

【 摘 要 】

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.

【 授权许可】

CC BY