ember 3 issue of the Journal of Clinical Investigation, Steven Ziegler and colleagues from the Benaroya Research Institute in Seattle report that CD25-CD4+ T cells produced in the thymus can differentiate to Foxp3-expressing CD25+CD4+ T regulatory cells in the periphery and are capable of suppressing the activation and expansion of self-reactive T cells that may cause autoimmune disease. The report suggests an active role for Foxp3 in suppressing self-directed immune responses and a therapeutic role for Foxp3 in the treatment of autoimmune diseases.

In an accompanying commentary in the same issue, Shimon Sakaguchi from Kyoto University, Japan, discusses the developmental pathway of Foxp3-expressing T regulatory cells and their role in controlling self-tolerance and autoimmunity.

TITLE: Induction of FoxP3 and acquisition of T regulatory activity by stimulated human CD4+Cd25- T cells.

AUTHOR CONTACT:
Steven F. Ziegler
Benaroya Research Institute, Seattle, Washington, USA.
Phone: 206-344-7950
Fax: 206-223-7543
E-mail: sziegler@benaroyaresearch.org

View the PDF of this article at: https://www.the-jci.org/press/19441.pdf

ACCOMPANYING COMMENTARY:
The origin of FOXP3-expressing CD4+ regulatory T cells: thymus or periphery

AUTHOR CONTACT:
Shimon Sakaguchi
Institute for Frontier Medical Sciences, Kyoto University, Kyoto, Japan.
Phone: 81-75-751-3888
Fax: 81-75-751-3820
E-mail: shimon@frontier.kyoto-u.ac.jp

View the PDF of this commentary at: https://www.the-jci.org/press/20274.pdf

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Contact: Brooke Grindlinger
science_editor@the-jci.org
212-342-9006
Journal of Clinical Investigation
3-Nov-2003

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