Abstract

Both genetic and environmental factors play a role in the development of type 1 diabetes, an autoimmune disease where the pancreatic insulin producing beta cells are destroyed by the immune system. Type 1 diabetes, a disease of juvenile onset, was lethal before the discovery of insulin in the 1920s and is dramatically increasing in incidence in the developed world. This increase is occurring faster than can be accounted for by genetic change. There has been considerable interest in determining the role that infection might play in the development of autoimmune diabetes. Initial studies focused on the role that infection might play in precipitating diabetes onset but more recently there has been an increased focus on the ways in which infections might inhibit the development of this autoimmune disease. This is particularly relevant since some infectious agents have co-evolved with the human immune system and indeed some use the human immune system to facilitate their life cycle. The relationships between humans and infectious agents of historical importance have been perturbed with improved housing, sanitation and the advent of vaccination strategies.

By using the NOD mouse model of type 1 diabetes it has been possible to show that some, but not all infections, are able to provide long term protection against diabetes development. The ways in which infectious agents modulate diabetes onset include effects on the innate and the adaptive immune response. Different infections such as helminth, viral or bacterial can modulate onset of diabetes through different mechanisms. In some cases diabetes prevention can be achieved using microbially derived products obviating the need for a live infection. The ways in which these agents or their products mediate diabetes prevention will be discussed.