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JCI table of contents: Dec. 22, 2010
Date:12/22/2010

p>TITLE: The TNFR family members OX40 and CD27 link viral virulence to protective T cell vaccines in mice

AUTHOR CONTACT:
Shahram Salek-Ardakani
La Jolla Institute for Allergy and Immunology, La Jolla, California, USA.
Phone: 858.752.6752; Fax: 858.752.6985; E-mail: ssalek@liai.org.

Michael Croft
La Jolla Institute for Allergy and Immunology, La Jolla, California, USA.
Phone: 858.752.6752; Fax: 858.752.6985; E-mail: mick@liai.org.

View this article at: http://www.jci.org/articles/view/42056?key=5097f4ccc796cf805ed2

ACCOMPANYING COMMENTARY
TITLE: A stimulating way to improve T cell responses to poxvirus-vectored vaccines

AUTHOR CONTACT:
Stuart N. Isaacs
University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA.
Phone: 215.662.2150; Fax: 215.349.5111; E-mail: isaacs@mail.med.upenn.edu.

View this article at: http://www.jci.org/articles/view/45726?key=9f291f3dbddc87be69b3


HEMATOLOGY: What happens when Fanconi anemia cells overcome checkpoint arrest

The rare genetic disorder Fanconi anemia is associated with depletion of bone marrow cells, which leads to bone marrow failure, and a strong predisposition to cancer. The main cause of death for individuals with Fanconi anemia is bone marrow failure. However, a small proportion of individuals do not develop severe bone marrow failure and they live longer than others. A team of researchers, led by Jean Soulier, at Saint-Louis Hospital, France, has now identified a mechanism by which some patients become clinically stable.

In individuals with Fanconi anemia, the bone marrow cells become depleted
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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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