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JCI table of contents: August 17, 2006

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PTEN: the Treg's handbrake

Naturally occurring CD4+CD25+ Tregs are a specialized subpopulation of T cells that function to prevent other T cells destroying self-tissues. But harnessing the therapeutic potential of Tregs -- for example, to treat autoimmune diseases such as diabetes and rheumatoid arthritis -- is hampered by problems generating sufficient cells to be therapeutically effective. This is because, unlike non-regulatory T cells, Tregs do not proliferate in vitro when stimulated through either their TCR or IL-2 receptor alone.

Now, in a study appearing online on August 17 in advance of print publication in the September issue of the Journal of Clinical Investigation, Laurence Turka and colleagues from the University of Pennsylvania have shown that Tregs from mice with T cells that lack phosphatase and tensin homolog (PTEN) proliferate in response to IL-2. Importantly, PTEN-deficient Tregs retained their suppressive function in vitro and in vivo, indicating that loss of PTEN by Tregs only affects their proliferative capabilities in response to IL-2 and not their other functions. These results identify PTEN as a key protein that regulates the lack of responsiveness of Tregs to IL-2 and could provide researchers with a way to overcome one of the biggest obstacles to harnessing their therapeutic potential.

TITLE: PTEN inhibits IL-2 receptormediated expansion of CD4+CD25+ Tregs

AUTHOR CONTACT:
Laurence A. Turka
University of Pennsylvania
Philadelphia, Pennsylvania, USA
Phone: (215) 898-1018
Fax: (215) 573-2880
E-mail: turka@mail.med.upenn.edu.

View the PDF of this article at: https://www.the-jci.org/article.php?id=28057

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Contact: Karen Honey
press_releases@the-jci.org
212-342-4159
Journal of Clinical Investigation
17-Aug-2006


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