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JCI table of contents: Dec. 3, 2007
Date:12/3/2007

tes and rheumatoid arthritis (RA) are caused when immune cells known as lymphocytes attack our own body tissues. Depletion of the B cell subset of lymphocytes using an antibody specific for the protein CD20 has been shown to be effective for the treatment of RA. The effectiveness of such an approach for the treatment of type I diabetes is not known, largely because the reagents to address this question in preclinical models have been lacking. This problem has now been overcome by Li Wen and colleagues from Yale School of Medicine, New Haven, who have developed the necessary tools and shown that depletion of B cells can both prevent diabetes and reverse established disease in mice. In the accompanying commentary, Hlne Bour-Jordan and Jeffrey Bluestone from the University of California, San Francisco, highlight the importance of these advances for developing and optimizing the potential of CD20-specific antibodies for the treatment of type 1 diabetes.

In the study, autoimmune diabetessusceptible mice were engineered such that their B cells expressed human CD20. Depletion of B cells in these mice before they showed signs of diabetes, using a single dose of a CD20-specific antibody, delayed and/or reduced the onset of disease. Similarly, in mice already showing signs of diabetes, a single dose of the CD20-specific antibody reversed disease in a substantial proportion of the mice. Furthermore, the mechanism behind the protection afforded by CD20-specific antibody treatment was shown to be associated with increased numbers of regulatory T cells and B cells.

TITLE: Treatment with CD20-specific antibody prevents and reverses autoimmune diabetes in mice

AUTHOR CONTACT:
Li Wen
Yale School of Medicine, New Haven, Connecticut, USA.
Phone: (203) 785-7186; Fax: (203) 737-5558; E-mail: li.wen@yale.edu.

View the PDF of this article at: https
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Contact: Karen Honey
press_releases@the-jci.org
215-573-1850
Journal of Clinical Investigation
Source:Eurekalert

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