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JCI table of contents, January 2, 2004

eptor

AUTHOR CONTACT:
Mitchell A. Lazar
University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA.
Phone: 215-898-0198
Fax: 215-898-5408
E-mail: lazar@mail.med.upenn.edu

View the PDF of this commentary at: https://www.the-jci.org/press/20661.pdf

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A viral cure for type 1 diabetes

Viruses can both cause and prevent autoimmune disease. In order to understand this dualism, Matthias von Herrath and colleagues from the La Jolla Institute for Allergy and Immunology in California exposed prediabetic mice to viral infections. In the January 2 issue of the Journal of Clinical Investigation the authors report that infection with lymphocytic choriomeningitis virus (LCMV) during the prediabetic period completely abolished the diabetic process in two distinct mouse models.

This protection against the development of type 1 diabetes correlated with a reduced number of autoaggressive CD8 T cells in pancreatic islets. Increased production of the chemokine CXCL-10 in pancreatic lymph nodes redirected cells of the immune response away from the beta cells. Once in the pancreatic lymph node, CD8 lymphocytes underwent increased apoptosis, which was directly dependent on TNF-alpha and indirectly on IFN-gamma production. The data indicate that proinflammatory cytokines and chemokines induced by viral infection can influence ongoing autoaggressive processes beneficially at the preclinical stage if produced at the correct time, location, and level. Therefore viruses that do not directly destroy beta cells may actually enhance the course of autoimmune diabetes.

TITLE: Cure of prediabetic mice by viral infections involves lymphocyte recruitment along an IP-10 gradient

AUTHOR CONTACT:
Matthias von Herrath
La Jolla
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Contact: Brooke Grindlinger
science_editor@the-jci.org
212-342-9006
Journal of Clinical Investigation
2-Jan-2004


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