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.
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