Intercellular communication for innate immunity

Tan A Nguyen; Ken C Pang; Seth L Masters

doi:10.1016/j.molimm.2016.10.002

Intercellular communication for innate immunity

Mol Immunol. 2017 Jun:86:16-22. doi: 10.1016/j.molimm.2016.10.002. Epub 2016 Oct 18.

Authors

Tan A Nguyen¹, Ken C Pang², Seth L Masters³

Affiliations

¹ 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.
² 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.
³ 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.

PMID: 27769523
DOI: 10.1016/j.molimm.2016.10.002

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.

Keywords: Exosomes; Inflammasome; Innate immunity; Intercellular transfer; STING; Type I interferon.

Publication types

Review

MeSH terms

Bystander Effect / immunology*
Exosomes / metabolism
Humans
Immunity, Innate*
Inflammasomes / metabolism
Intercellular Junctions / immunology
Intercellular Junctions / metabolism
Interferon Type I / metabolism
Membrane Proteins / metabolism
Pathogen-Associated Molecular Pattern Molecules / immunology*
Receptors, Pattern Recognition / metabolism
Virus Diseases / immunology
Virus Diseases / metabolism
Viruses / immunology

Substances

Inflammasomes
Interferon Type I
Membrane Proteins
Pathogen-Associated Molecular Pattern Molecules
Receptors, Pattern Recognition
STING1 protein, human