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JCI online early table of contents: Nov. 14, 2011
Date:11/14/2011

ref="mailto:syevans@ucsd.edu">syevans@ucsd.edu.

View this article at: http://www.jci.org/articles/view/59472?key=71e79270eae8087e1de5

AUTOIMMUNITY: Linking genetic variants to autoimmune disease

Genetic studies have linked numerous genetic variations to susceptibility to developing an autoimmune disease. However, the functional consequences of most of these genetic variations remain unknown. Among the genes with variations linked to autoimmune diseases, including type 1 diabetes, rheumatoid arthritis, and Crohn's disease, is PTPN2, which templates a protein known as TCPTP. A team of researchers led by Tony Tiganis, at Monash University, Australia, has now identified a new immune function for TCPTP that might explain the link between PTPN2 genetic variations and autoimmune diseases.

In an accompanying commentary, Arthur Weiss and Julie Zikherman, at the University of California San Francisco, discuss how important it is to unravel the functional implications of genetic analyses so as to further understanding of the mechanisms underlying human autoimmune diseases.

TITLE: T cell protein tyrosine phosphatase attenuates T cell signaling to maintain tolerance in mice

AUTHOR CONTACT:
Tony Tiganis
Monash University, Clayton, Victoria, Australia.
Phone: 61-3-9902-9332; Fax: 61-3-9902-9500; E-mail: Tony.Tiganis@med.monash.edu.au.

View this article at: http://www.jci.org/articles/view/59492?key=e7f6a68a143397557389

ACCOMPANYING COMMENTARY

TITLE: Unraveling the functional implications of GWAS: how T cell protein tyrosine phosphatase drives autoimmune disease

AUTHOR CONTACT:
Arthur Weiss
University of California San Francisco, San Francisco, California, U
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Contact: Karen Honey
press_releases@the-jci.org
734-546-5242
Journal of Clinical Investigation
Source:Eurekalert

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