Infection by various viral and bacterial pathogens has long been proposed as one of the etiologies of autoimmune diabetes. Many theories, ranging from direct cytolysis of pancreatic islet cells to immunological processes such as antigen mimicry and polyclonal lymphocyte activation, tried to explain the epidemiological correlation between infections and diabetes, supported by information from human and animal studies. However, a direct correlation and exact mechanism continue to elude investigators due to scarce and conflicting data. Interestingly, there is also data to support an opposite role for infection in the development of type 1 diabetes, as several pathogens demonstrated a protective effect from this disease. This article reviews the current data available from clinical studies and animal models, while trying to explain the different mechanisms underlying these findings.
- Type 1 diabetes