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JCI online early table of contents: March 14, 2011
Date:3/14/2011

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TITLE: Lipid Profiling Identifies a Triacylglycerol Signature of Insulin Resistance and Improves Diabetes Prediction in Humans

AUTHOR CONTACT:
Robert Gerszten
Massachusetts General Hospital, Charlestown, MA, USA
Phone: 617-724-8322; Fax: 617-726-1544; E-mail: RGERSZTEN@PARTNERS.ORG

View this article at: http://www.jci.org/articles/view/44442?key=2db0a8efbc938e79f05b


IMMUNOLOGY Virus sensors help prevent type 1 diabetes

Type 1 diabetes (T1D) is a failure to maintain normal blood sugar levels due to death of the insulin-producing pancreatic β cells, most often resulting from autoimmune T cell-mediated attack. Multiple genetic variants have been found to be associated with the disease, and recent studies have also suggested that viral infection may contribute to the development of T1D. However, it is unclear whether viral infection of β cells results in direct damage, or whether the immune response to the virus initiates a T cell-mediated β cell killing.

In this paper, Marco Colonna and colleagues, at Washington University School of Medicine in St. Louis, Missouri, investigated the role of the immune response in a mouse model of virally-induced T1D. They found that two genes involved in helping cells recognize invading viruses, toll like receptor 3 (Tlr3) and melanoma differentiation-associated gene 5 (Mda5), were important in protecting infected mice from developing T1D. In mice lacking those genes, the virus was better able to infect and kill β cells. The researchers believe that these findings suggest that the immune system can both promote and prevent T1D, depending on the underlying pathology in the patient.

TITLE: RNA sensorinduced type I IFN prevents diabetes caused by a β celltropic virus in mice

AUTHOR CONTACT:
Marco Colonna
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Contact: Kathryn Claiborn
press_releases@the-jci.org
Journal of Clinical Investigation
Source:Eurekalert

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