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 b cells. Once in the pancreatic lymph node, CD8 lymphocytes underwent increased apoptosis, which was directly dependent on TNF-a and indirectly on IFN-g 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 b 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 Institute for Allergy and Immunology, San Diego, California, USA.
Phone: 858-558-3571
Fax: 858-558-3579
E-mail: matthias@liai.org
View the PDF of this article at: http://www.jci.org/cgi/content/full/113/1/74
Journal of Clinical Investigation