title: Intercellular communication for innate immunity.
abstract: An effective innate immune response relies on the detection of pathogen associated molecular patterns (PAMPs) by various host pattern recognition receptors (PRRs) that result in the production of pro-inflammatory cytokines and chemokines. Viruses and bacteria have co-evolved with the immune system and developed multiple strategies to usurp or circumvent host machinery and blunt the innate immune response in infected cells. Recently, it has become apparent that infected or dying cells can transmit PAMPs and host PRR signalling proteins to uninfected bystander cells to thereby bypass pathogen evasion strategies, and potentiate innate immune signalling. This bystander activation of innate immunity represents an alternative method by which the host can control infections via cell-to-cell communication. In this review, we discuss what is currently known about the intercellular transfer of pathogen- or host-derived RNA, DNA and proteins from infected cells to neighbouring cells and how this impacts on host innate immunity.
authors: Inflammation Division, The Walter and Eliza Hall Institute of Medical Research, Parkville 3052, Australia; Department of Medical Biology, The University of Melbourne, Parkville 3010, Australia. Electronic address: nguyen.t@wehi.edu.au.
authors: Tan A
authors: TA
authors: Nguyen
authors: Inflammation Division, The Walter and Eliza Hall Institute of Medical Research, Parkville 3052, Australia; Murdoch Children's Research Institute, Parkville, VIC, Australia; Department of Paediatrics, University of Melbourne, Parkville, VIC, Australia; Department of Psychiatry, University of Melbourne, Parkville, VIC, Australia.
authors: Ken C
authors: KC
authors: Pang
authors: Inflammation Division, The Walter and Eliza Hall Institute of Medical Research, Parkville 3052, Australia; Department of Medical Biology, The University of Melbourne, Parkville 3010, Australia.
authors: Seth L
authors: SL
authors: Masters
mesh_terms: D024201:Bystander Effect / Q000276:immunology*; D055354:Exosomes / Q000378:metabolism; D006801:Humans; D007113:Immunity, Innate; D058847:Inflammasomes / Q000378:metabolism; D007365:Intercellular Junctions / Q000276:immunology / Q000378:metabolism; D007370:Interferon Type I / Q000378:metabolism; D008565:Membrane Proteins / Q000378:metabolism; D000069452:Pathogen-Associated Molecular Pattern Molecules / Q000276:immunology*; D051192:Receptors, Pattern Recognition / Q000378:metabolism; D014777:Virus Diseases / Q000276:immunology / Q000378:metabolism; D014780:Viruses / Q000276:immunology; D000099197:STING Protein
chemical_list: D058847:Inflammasomes; D007370:Interferon Type I; D008565:Membrane Proteins; D000069452:Pathogen-Associated Molecular Pattern Molecules; D051192:Receptors, Pattern Recognition; C532857:STING1 protein, human; D000099197:STING Protein
keywords: Exosomes; Inflammasome; Innate immunity; Intercellular transfer; STING; Type I interferon