Moynagh, Paul N. (2003) Toll-like receptor signalling pathways as key targets for mediating the anti-inflammatory and immunosuppressive effects of glucocorticoids. Journal of Endocrinology, 179 (2). pp. 139-144. ISSN 0022–0795

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Abstract

Toll-like receptors (TLRs) play crucial roles in the induction of innate immune responses by recognising pathogen-associated molecular patterns. The engagement of TLRs by pathogens results in induction of co-stimulatory molecules that facilitate a specific immune response and also in the induction of pro-inflammatory proteins that will promote the elimination of pathogens from the body. TLRs employ many of the same signalling components as the type I interleukin (IL)-1 receptor (IL-1R). This is hardly surprising since the intracellular regions of TLRs and the IL-1R share a conserved Toll/IL-1R homology domain (TIR) that allows the receptors to recruit the intracellular TIR-containing adaptor protein Myd88. The latter then activates IL-1R-associated kinases that in turn recruit well-characterised downstream effectors culminating in activation of MAP kinases and transcription factors such as NFkappaB and AP-1. Since glucocorticoids are known to target the latter transcription factors and the MAP kinase cascades, this commentary highlights the likely crucial importance of Toll-like receptor signalling pathways as key targets for mediating the anti-inflammatory and immunosuppressive effects of steroids.

Item Type:	Article
Keywords:	Toll-like receptor; signalling pathways; anti-inflammatory; immunosuppressive effects; glucocorticoids;
Academic Unit:	Faculty of Science and Engineering > Biology
Item ID:	7207
Identification Number:	https://doi.org/10.1677/joe.0.1790139
Depositing User:	Professor Paul Moynagh
Date Deposited:	20 Jul 2016 16:02
Journal or Publication Title:	Journal of Endocrinology
Publisher:	Society for Endocrinology
Refereed:	Yes
URI:	http://joe.endocrinology-journals.org/
Use Licence:	This item is available under a Creative Commons Attribution Non Commercial Share Alike Licence (CC BY-NC-SA). Details of this licence are available here

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