Abstract
G protein-coupled receptors (GPCRs) are a large family of transmembrane proteins that perceive many extracellular signals and transduce them into cellular physiological responses. GPCRs regulate immunity in both vertebrates and invertebrates. However, the mechanisms responsible for such regulation are not fully understood. Recent research using the genetically tractable model organism Caenorhabditis elegans has led to the identification of specific GPCRs, neurotransmitters, neurons and non-neural cells in the regulation of innate immunity. Several neural circuits have been demonstrated to function in GPCR-dependent immuno-regulatory pathways. Besides being essential in neural-immune interactions, GPCRs also regulate innate immune response in non-neural tissues cell-autonomously through mechanisms independent of neural circuits. Here we review GPCR-mediated neural control of innate immunity in C. elegans and briefly discuss GPCR-dependent immune regulation via non-neural mechanisms.
Highlights
G protein-coupled receptors (GPCRs) constitute the largest and most versatile superfamily of membrane bound signaling proteins
We demonstrated that C. elegans lacking OCTR -1, a octopamineGPCR, in two types of sensory neurons exhibited substantially improved survival against the human opportunistic pathogen Pseudomonas aeruginosa strain PA14 [10]
We further showed that neuronal OCTR-1 regulates the canonical unfolded protein response (UPR) pathway, which is controlled by the X-box binding protein 1 (XBP-1) [38, 39], at the organismal level [25]
Summary
G protein-coupled receptors (GPCRs) constitute the largest and most versatile superfamily of membrane bound signaling proteins. GPCRs either function in non-neural tissues to control innate immune responses or act in the nervous system to modulate immunity in a cell non-autonomous manner. Upon infection with microorganisms, including many human pathogens, C. elegans can mount innate immune responses by activating signaling pathways that are conserved in humans [33,34,35].
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