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JCI online early table of contents: Nov. 15, 2010
Date:11/15/2010


Institut Cochin, Universit Paris Descartes, CNRS, UMR 8104, INSERM, U1016, Paris, France.
Phone: 33.1.53.73.27.20; Fax: 33.1.53.73.27.03; Email: renaud.dentin@inserm.fr.

View this article at: http://www.jci.org/articles/view/41624?key=5a93c7622e5586b36422


AUTOIMMUNITY: Attacking the symptoms of SLE

Systemic lupus erythematosus (SLE) is a relatively common autoimmune disorder, i.e., a disorder caused by a person's immune system turning on that person's body and inflicting tissue damage. The disease can affect the skin, joints, kidneys, and other organs. There is no cure for SLE, although there are good treatments to combat many of the symptoms. A team of researchers, led by Liliana Schaefer, at the Institut fr Allgemeine Pharmakologie und Toxikologie/ZAFES, Germany, has now identified, through work in mice, a potential new target for treating the symptoms of SLE

One marker of disease activity in individuals with SLE is CXCL13, which is a protein that attracts immune cells known as B cells. The team has now identified a mechanism by which CXCL13 is induced in a mouse model of SLE. Specifically, increased levels of the molecule biglycan interacted with proteins known as TLR2/4 to trigger production of CXCL13. Importantly, biglycan deficiency was associated with reduced disease. Further, as levels of biglycan were elevated in patients with SLE, the authors suggest that targeting biglycan-TLR2/4 interactions might provide a new approach to treating the symptoms of SLE.

TITLE: The proteoglycan biglycan regulates expression of the B cell chemoattractant CXCL13 and aggravates murine lupus nephritis

AUTHOR CONTACT:
Liliana Schaefer
Institut fr Allgemeine Pharmakologie und Toxikologie/ZAFES, Frankfurt am Main, Germany.
Phone: 49.69.6301.7899; Fax: 49.69.6301
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Contact: Karen Honey
press_releases@the-jci.org
734-546-5242
Journal of Clinical Investigation
Source:Eurekalert

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