Save
Email
Print
ShareMay 28, 2009 — Type 1 diabetes is caused by immune system–mediated destruction of insulin-producing beta-cells in the pancreas. It is known that infection with a virus can induce an immune response that damages beta-cells or a response that protects an individual from type 1 diabetes.
However, the mechanisms by which viruses can have such divergent effects are not well understood. A team of researchers, at La Jolla Institute for Allergy & Immunology, La Jolla, has now provided some insight into this issue by showing that in a mouse model of type 1 diabetes, viruses that do not damage beta-cells provide protection from the autoimmune disease.
The team, led by Christophe Filippi and Matthias von Herrath, observed that infection with either Coxsackie virus B3 or lymphocytic choriomeningitis virus delayed the onset and reduced the incidence of disease in the mouse model of type 1 diabetes. Further analysis revealed a synergistic underlying protective mechanism: levels of the protein PD-L1 were transiently upregulated on immune cells known as lymphoid cells, and there was an increase in the number of CD4+CD25+ Tregs and an increase in their ability to produce the immunomodulatory factor TGF-beta.
In an accompanying commentary, Terry Strom, at Beth Israel Deaconess Medical Center, Boston, discusses these mechanisms in further detail.
Other social bookmarking and sharing tools:
Story Source:
The above story is reprinted from materials provided by Journal of Clinical Investigation, via EurekAlert!, a service of AAAS.
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
Journal References:
- Christophe Filippi et al. Immunoregulatory mechanisms triggered by viral infections protect from type 1 diabetes in mice. Journal of Clinical Investigation, May 26, 2009
- Terry Strom. Can childhood viral infection protect from type 1 diabetes? Journal of Clinical Investigation, May 26, 2009
Note: If no author is given, the source is cited instead.
more 
