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    Toll-like receptor signalling pathways as key targets for mediating the anti-inflammatory and immunosuppressive effects of glucocorticoids


    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:

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