Abstract

Recognition of the non-self signature of invading pathogens is a crucial step for the initiation of the innate immune mechanisms of the host. The host response to viral and bacterial infection involves sets of pattern recognition receptors (PRRs), which bind evolutionarily conserved pathogen structures, known as pathogen-associated molecular patterns (PAMPs). Recent advances in the identification of different types of PRRs in teleost fish revealed a number of cytosolic sensors for recognition of viral and bacterial nucleic acids. These are DExD/H-box RNA helicases including a group of well-characterized retinoic acid inducible gene I (RIG-I)-like receptors (RLRs) and non-RLR DExD/H-box RNA helicases (e.g., DDX1, DDX3, DHX9, DDX21, DHX36 and DDX41) both involved in recognition of viral RNAs. Another group of PRRs includes cytosolic DNA sensors (CDSs), such as cGAS and LSm14A involved in recognition of viral and intracellular bacterial dsDNAs. Moreover, dsRNA-sensing protein kinase R (PKR), which has a role in antiviral immune responses in higher vertebrates, has been identified in fish. Additionally, fish possess a novel PKR-like protein kinase containing Z-DNA binding domain, known as PKZ. Here, we review the current knowledge concerning cytosolic sensors for recognition of viral and bacterial nucleic acids in teleosts.

Highlights

  • The innate immune response relies on the recognition of evolutionarily conserved pathogen components, termed as pathogen-associated molecular patterns (PAMPs), through the germ line-encoded pattern recognition receptors (PRRs) [1]

  • Till five major groups of PRRs have been discovered: (i) Toll-like receptors (TLRs), (ii) nucleotide-binding oligomerization domain (NOD)-leucin rich repeats (LRR)-containing receptors (NLRs), (iii) retinoic acid-inducible gene 1 (RIG-1)-like receptors (RLRs or RIG-1-like helicases-RLH) which belongs to the large family of DExD/H-box RNA helicases, (iv) C-type lectin receptors (CLRs) and (v) cytosolic DNA sensors [2,3,4,5,6,7]

  • Over the past decade or so, several investigations have focused on clarifying the mechanisms underlying these innate immune responses triggered by sensors that recognize pathogen-derived components in cytosol

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Summary

Introduction

The innate immune response relies on the recognition of evolutionarily conserved pathogen components, termed as pathogen-associated molecular patterns (PAMPs), through the germ line-encoded pattern recognition receptors (PRRs) [1]. Till five major groups of PRRs have been discovered: (i) Toll-like receptors (TLRs), (ii) nucleotide-binding oligomerization domain (NOD)-leucin rich repeats (LRR)-containing receptors (NLRs), (iii) retinoic acid-inducible gene 1 (RIG-1)-like receptors (RLRs or RIG-1-like helicases-RLH) which belongs to the large family of DExD/H-box RNA helicases, (iv) C-type lectin receptors (CLRs) and (v) cytosolic DNA sensors [2,3,4,5,6,7] They can be found associated to subcellular compartments–cellular and endosomal membranes, in the cytosol, as well as extracellularly and in secreted forms present in the bloodstream and interstitial fluids [8]. In specific cases, PRRs recognize self-danger signals (DAMPs, damage/danger associated molecular patterns), which are present in abnormal locations or atypical molecular complexes as a consequence of infection/inflammation, or cellular stress [9,10]

Viral and Bacterial PAMPs and Their PRRs
Receptor Structure
Ligands
Signal Transduction
RLRs in Fish
LSm14A
PKR and PKZ
Findings
10. Conclusions

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