Type I diabetes is an autoimmune disease involving an interaction betw
een an epigenetic event (possibly a viral infection), the pancreatic b
eta cells, and the immune system in a genetically susceptible host. Th
e possibility that the type I interferons could mediate this interacti
on was tested with transgenic mice in which the insulin-producing beta
cells expressed an interferon-alpha. These mice developed a hypoinsul
inemic diabetes associated with a mixed inflammation centered on the i
slets. The inflammation and the diabetes were prevented with a neutral
izing antibody to the interferon-alpha. Thus, the expression of interf
eron-alpha by the beta cells could be causal in the development of typ
e I diabetes, which suggests a therapeutic approach to this disease.