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Int Rev Immunol. 2017 Mar 4;36(2):74-88. doi: 10.1080/08830185.2017.1298749. Epub 2017 Mar 23.

Cytosolic nucleic acid sensors and innate immune regulation.

Author information

1
a Laboratory of Molecular Immunobiology , Graduate School of Biological Sciences, Nara Institute of Science and Technology (NAIST), Takayama-cho , Ikoma , Nara , Japan.

Abstract

During viral and bacterial infections, pathogen-derived cytosolic nucleic acids are recognized by the intracellular RNA sensors retinoic acid-inducible gene I and melanoma-differentiated gene 5 and intracellular DNA sensors, including cyclic-di-GMP-AMP synthase, absent in melanoma 2, interferon (IFN)-gamma inducible protein 16, polymerase III, and so on. Binding of intracellular nucleic acids to these sensors activates downstream signaling cascades, resulting in the production of type I IFNs and pro-inflammatory cytokines to induce appropriate systematic immune responses. While these sensors also recognize endogenous nucleic acids and activate immune responses, they can discriminate between self- and non-self-nucleic acids. However, dysfunction of these sensors or failure of regulatory mechanisms causes aberrant activation of immune response and autoimmune disorders. In this review, we focus on how intracellular immune sensors recognize exogenous nucleic acids and activate the innate immune system, and furthermore, how autoimmune diseases result from dysfunction of these sensors.

KEYWORDS:

DNA sensors; Immunity; RNA sensors; innate immunity; intracellular nucleic acid

PMID:
28333574
DOI:
10.1080/08830185.2017.1298749
[Indexed for MEDLINE]

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