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JCI online early table of contents: Oct. 18, 2010
Date:10/18/2010

desmoglein proteins that are key to maintaining the integrity of the skin.

A team of researchers, led by John Stanley, at the University of Pennsylvania, Philadelphia, set out to understand whether the antibodies that cause disease in different patients share any features that could ultimately be targeted by a specific therapy. Analysis of the disease-causing antibodies from 5 patients indicated that a region of these antibodies known as the H-CDR3 shared a similar amino-acid sequence (i.e., the protein building blocks making up this region of the antibody were similar). Importantly, changing the building blocks in H-CDR3 eliminated their ability to cause blistering in human skin organ cultures. Thus, the team suggests that targeting therapy to the H-CDR3 might reduce the ability of the pemphigus-causing antibodies to elicit disease.

TITLE: Homologous regions of autoantibody heavy chain complementarity-determining region 3 (H-CDR3) in patients with pemphigus cause pathogenicity

AUTHOR CONTACT:
John R. Stanley
University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Phone: 215.898.3240; Fax: 215.573.2033; E-mail: jrstan@mail.med.upenn.edu.

View this article at: http://www.jci.org/articles/view/44425?key=cb0bebbcdf1456d7f6b4


CARDIOLOGY: Genetic inactivation fails to confirm role for microRNA-21 in heart failure

Persistent high blood pressure puts stress on the heart, which responds by remodeling its walls to withstand the extra pressure. This remodeling can lead to heart failure. It is hoped that identifying the key molecules that induce this remodeling will provide new therapeutic targets. Recent data suggest that a therapeutic (specifically an antagomir) that inhibits a molecule known as miR-21 alleviates remodeling and heart failure in a rodent model o
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Contact: Karen Honey
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Journal of Clinical Investigation
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