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JCI online early table of contents: Sept. 1, 2010
Date:9/1/2010

e absence of invading microbes so that they do not cause unwanted tissue damage. Indeed, dysfunction of proteins that negatively regulate the alternative pathway of complement activation has been linked to several human inflammatory disorders. Wen-Chao Song and colleagues, at the University of Pennsylvania School of Medicine, Philadelphia, have now determined that the protein properdin has a key role in tissue injury caused by alternative pathway complement activation in mice. For example, properdin deficiency reduced the severity of disease in a mouse model of arthritis. The authors therefore suggest that targeting properdin could be a way to treat human inflammatory diseases caused by alternative pathway complement activation.

TITLE: Genetic and therapeutic targeting of properdin in mice prevents complement-mediated tissue injury

AUTHOR CONTACT:
Wen-Chao Song
University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA.
Phone: 215.573.6641; Fax: 215.746.8941; E-mail: songwe@upenn.edu.

View this article at: http://www.jci.org/articles/view/41782?key=586c429ae17e0189f66f


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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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