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Autoimmune type 1 diabetes is caused by an interactive combination of genetic and environmental factors, most of which remain unknown. Each individual appears to have a unique combination of these factors that allow for their susceptibility to disease. Investigators have long searched for physiological mechanisms that could link diverse environmental events to inheritable genetic traits and the aberrant gene expression in immune cells. Much of this search has focused on either uncovering elusive gene polymorphisms found in at-risk populations or on finding common elements in the lives of susceptible individuals that “trigger” their immune system toward a self-destructive path (1,2). To date, only a few gene polymorphisms have linked to susceptibility, with none so far proven both essential and sufficient to promote disease (1). The search for environmental etiological agents in this multifactorial disease has been no less difficult, since each individual afflicted appears to have a unique set of factors promoting autoimmunity rather than a single or few common triggers (2). So how can such a diverse set of environmental stimulators rapidly and reversibly trigger a variety of undefined genetic regions to promote the loss of something as basic to normal physiology as tolerance of self? Is there a common mechanism even when the end targets are elusive and environmental slings and arrows are so diverse? Enter epigenetic gene regulation into the tableau, adding a …

Immunopathogenic Interaction of Environmental Triggers and Genetic Susceptibility in Diabetes