Display Settings:

Format

Send to:

Choose Destination
See comment in PubMed Commons below
Cytokine. 2012 Aug;59(2):195-202. doi: 10.1016/j.cyto.2012.04.003. Epub 2012 May 12.

Toll-like receptor signalling in liver disease: ER stress the missing link?

Author information

  • 1Experimental Medicine Group, UCD School of Medicine and Medical Science, Mater Misericordiae University Hospital, Dublin, Ireland. matthew.lawless1@gmail.com

Abstract

Toll-like receptors induce a complex inflammatory response that can function to alert the body to infection, neutralize pathogens and repair damaged tissues. Toll-like receptors are expressed on kupffer, endothelial, dendritic, biliary epithelial, hepatic stellate cells, and hepatocytes in the liver. The endoplasmic reticulum (ER) is a central organelle of eukaryotic cells that exists as a place of lipid synthesis, protein folding and protein maturation. The ER is a major signal transduction organelle that senses and responds to changes in homeostasis. Conditions interfering with the function of the ER are collectively known as ER stress and can be induced by accumulation of unfolded protein aggregates or by excessive protein traffic as can occur during viral infection. The ability of ER stress to induce an inflammatory response is considered to play a role in disease pathogenesis. Importantly, ER stress is viewed as a contributor to the pathogenesis of liver diseases with evidence linking components of ER homeostasis as requirements for optimal Toll-like receptor function. In this context this review discusses the association of Toll-like receptors with ER stress. This is an emerging paradigm in the understanding of Toll-like receptor signalling which may have an underlying role in the pathogenesis of liver disease.

Copyright © 2012 Elsevier Ltd. All rights reserved.

PMID:
22579700
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Write to the Help Desk