Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.

Subscribe

Sci. STKE, 8 August 2000
Vol. 2000, Issue 44, p. re1
[DOI: 10.1126/stke.442000re1]

REVIEWS

The Interleukin-1 Receptor/Toll-like Receptor Superfamily: Signal Transduction During Inflammation and Host Defense

Luke A. J. O'Neill

The author is in the Department of Biochemistry and Biotechnology Institute, Trinity College, Dublin, Ireland. E-mail: laoneill{at}tcd.ie

Gloss: The interleukin-1 (IL-1) receptor/Toll-like receptor superfamily plays a central role in inflammation and the host response to bacterial infection. It includes receptors for the cytokines IL-1 and IL-18, which are induced during inflammation and in response to microbial products during infection. Products released by Gram-positive and Gram-negative bacteria, acting via the Toll-like receptors TLR-2 and TLR-4, respectively, provoke host defenses that eliminate such bacteria. Members occur in diverse species, including mammals, plants, and insects; in insects, receptors such as Toll are also involved in development. The Toll-IL-1 receptor (TIR) domain occurs in the cytosolic region of all superfamily members and triggers the activation of transcription factors such as nuclear factor {kappa}B (NF-{kappa}B), and also activates the mitogen-activated protein kinases (MAPKs) p38 and c-Jun NH2-terminal kinase (JNK). These signals lead to the increased expression of proteins involved in immunity and inflammation, thereby leading to the elimination of infectious agents, or to chronic inflammation in autoimmune diseases. NF-{kappa}B binding sites occur in the promoters of a large number of immune genes, and the signaling pathway to NF-{kappa}B is known in detail. The IL-1 receptor/Toll-like receptor system is therefore evolutionarily conserved and is a critical determinant of innate immune and inflammatory responses.

Citation: L. A. J. O'Neill, The Interleukin-1 Receptor/Toll-like Receptor Superfamily: Signal Transduction During Inflammation and Host Defense. Sci. STKE 2000, re1 (2000).


THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
TLR5-mediated activation of p38 MAPK regulates epithelial IL-8 expression via posttranscriptional mechanism.
Y. Yu, H. Zeng, S. Lyons, A. Carlson, D. Merlin, A. S. Neish, and A. T. Gewirtz (2003)
Am J Physiol Gastrointest Liver Physiol 285, G282-G290
   Abstract »    Full Text »    PDF »

To Advertise     Find Products


Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882