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JCI table of contents, 17 May 2004

the initial step of septic inflammation. They showed that use of antibodies against the toll-like receptor 2 (TLR2) in lipopeptide-challenged mice blocked the release of markers of the inflammatory response, such as TNFa, and protected the mice from a lethal shock-like syndrome. The results here indicate the potential suitability for antibody-directed therapy in treating septic shock.

An accompanying commentary by Thomas Decker, of the University of Vienna, provides an overview of Toll-like receptors, their role in bacterial infection, and a discussion of the potential strengths and weaknesses of targeting these receptors for combating sepsis.

TITLE: Antagonistic antibody prevents toll-like receptor 2driven lethal shock-like syndromes

AUTHOR CONTACT:
Carsten J. Kirschning
Technical University of Munich, Munich, Germany.
Phone: 49-89-4140-4132; Fax: 49-89-4140-4139; E-mail: carsten.kirschning@lrz.tum.de

View the PDF of this article at: https://www.the-jci.org/press/20762.pdf

ACCOMPANYING COMMENTARY: Sepsis: avoiding its deadly toll

AUTHOR CONTACT:
Thomas Decker
University of Vienna, Vienna, Austria.
Phone: 43-1-4277-54605; Fax: 43-1-4277-9546; E-mail: thomas.decker@univie.ac.at

View the PDF of this commentary at: https://www.the-jci.org/press/21819.pdf

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Bile Keeps Triglycerides Down

Elevated triglyceride (TG) levels have been shown to be a cardiovascular disease risk factor. TG production is controlled largely at the transcriptional level by the transcription factor SREBP-1c, which governs fatty acid synthesis. TG levels are also inversely affected by bile acids, although the mechanism underlying
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Contact: Laurie Goodman
press_releases@the-jci.org
212-342-4159
Journal of Clinical Investigation
17-May-2004


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