A Designer Approach To Regulating Autoimmunity In Diabetes
Main Category: DiabetesAlso Included In: Immune System / Vaccines
Article Date: 06 Aug 2006 - 2:00 PDT
Type 1 diabetes is an autoimmune disorder in which the body's own immune system attacks the beta cells of the pancreas, destroying or damaging them sufficiently to reduce or impair insulin production. Therefore, shutting down the autoreactive T cells that attack beta islet cells is one therapeutic approach that researchers have been investigating. A molecule named cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) is known to prevent T cell activation from getting out of control and as such researchers have been trying to identify ways in which to selectively engage and activate CTLA-4 to treat diabetes. In a study appearing in the August issue of the Journal of Clinical Investigation, Jeffrey Bluestone and colleagues from the University of California, San Francisco, designed and developed a transgenic mouse expressing an anti-CTLA-4 antibody on B cells that was capable of selectively inhibiting activated T cells and T cell-dependent B cell responses and prevented autoimmune diabetes in these animals. The study suggests that selective engagement of CTLA-4 in this manner represents a novel immunotherapeutic approach to the treatment of type 1 diabetes.
In an accompanying commentary, Mohamed H. Sayegh from Harvard Medical School discusses the potential harnessing of this "designer" approach for the prevention or cure of autoimmune diabetes.
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Article adapted by Medical News Today from original press release.
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TITLE: Inhibition of T cell activation and autoimmune diabetes using a B cell surface-linked CTLA-4 agonist
AUTHOR CONTACT:
Jeffrey A. Bluestone
University of California, San Francisco, California, USA.
E-mail: jbluest@diabetes.ucsf.edu.
View the PDF of this article at: http://https://www.the-jci.org/article.php?id=27856
ACCOMPANYING COMMENTARY
TITLE: Costimulation couture: a designer approach to regulating immunity
AUTHOR CONTACT:
Mohamed H. Sayegh
Harvard Medical School, Boston, Massachusetts, USA.
E-mail: msayegh@rics.bwh.harvard.edu.
View the PDF of this article at: http://https://www.the-jci.org/article.php?id=29455
Source: JCI table of contents: August, 2006
Contact: Brooke Grindlinger
Journal of Clinical Investigation
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