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, 7 August 2007
Vol. 2007, Issue 398, p. tw286
[DOI: 10.1126/stke.3982007tw286]

EDITORS' CHOICE

Immunology Keeping Tabs on a TLR Response

Stephen J. Simpson

Science, AAAS, Cambridge CB2 1LQ, UK

Toll-like receptors (TLRs) exert powerful proinflammatory responses to microbial pathogens, and TLR responses are stringently regulated during infection so that the chronic exposure of cells to microbial products can ultimately lead to a state of hyporesponsiveness. Carmody et al. identify an essential role for the proto-oncogene protein B cell leukemia (Bcl)-3 in negatively regulating TLR signaling in this context. Bcl-3 blocks ubiquitination of the nuclear factor {kappa}B subunit p50, which prevents its degradation and allows it to maintain its inhibition of gene transcription in response to TLR signals. This pathway offers a means by which microbial signals can be prevented from overpowering the immune response.

R. J. Carmody, Q. Ruan, S. Palmer, B. Hilliard, Y. H. Chen, Negative regulation of Toll-like receptor signaling by NF-{kappa}B p50 ubiquitination blockade. Science 317, 675-678 (2007). [Abstract] [Full Text]

Citation: S. J. Simpson, Keeping Tabs on a TLR Response. Sci. STKE 2007, tw286 (2007).


To Advertise     Find Products


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