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JCI early table of contents for Feb. 8, 2013
Date:2/8/2013

disease progression. Additionally, they identified small proteins that induced more CD8+ Tregs. These findings suggest that enhancing specific T cell subsets may be useful in combating RA and other autoimmune diseases.

TITLE:

Amelioration of arthritis through mobilization of peptide-specific CD8+ regulatory T-cells

AUTHOR CONTACT:
Harvey Cantor
Dana Farber Cancer Institute, Boston, MA, USA
Phone: 617-632-3348; Fax: 617-632-4630; E-mail: harvey_cantor@dfci.harvard.edu

View this article at: http://www.jci.org/articles/view/66938?key=921590f51ca9f29cbc53


New insight into RASopathy-associated lymphatic defects

The RAS pathway is a cellular signaling pathway that regulates growth and development in humans. RASopathies are a group of diseases characterized by defects in RAS signaling. Many patients with RASopathies present with defects in the lymphatic system, which removes excess fluid from tissues, absorbs fats from the digestive system, and transports immune cells. To determine how alterations in the RAS pathway affect development of the lymphatic system, researchers at Yale University generated transgenic mice that expressed mutations associated with a RASopathy known as Noonan syndrome. In this issue of the Journal of Clinical Investigation, Michael Simon and colleagues report that excess RAS pathway activation triggers increased activity of a protein known as ERK. Mice with RASopathy-associated mutations exhibited lymphatic defects similar to those seen in humans, but the defects could be reversed by treatment with an ERK inhibitor. These findings demonstrate that excessive ERK activation underlies lymphatic defects in RASopathies and suggest that ERK inhibition could be a useful therapeutic strategy.

TITLE:
Endothelial ERK
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Contact: Jillian Hurst
press_releases@the-jci.org
Journal of Clinical Investigation
Source:Eurekalert

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