Prevention of Autoimmune Disease: Type 1 Diabetes as a Paradigm

Publisher Summary

It is noted that in the case of type 1 diabetes (T1D) the disease process begins months to years before major loss of beta-cell function heralds symptoms of hyperglycemia. Increasing knowledge of the mechanisms of beta-cell destruction and the ability to identify individuals at risk for T1D, together with proof-of-principle for therapeutic intervention in the non-obese diabetic (NOD) mouse model, are platforms for T1D prevention in humans. Indeed, T1D can be seen as a paradigm for the preclinical diagnosis and prevention of autoimmune disease in general. Preventing T1D applies not only to people at risk but also to those with clinical diabetes, in order to preserve residual beta-cell function, allow possible beta-cell regeneration and prevent recurrent autoimmune disease after therapeutic betacell replacement or regeneration. Furthermore, T1D can be eradicated by primary prevention aimed at avoiding or averting the environmental factors that are thought to precipitate disease in genetically at-risk individuals. Prevention is, however, mostly applicable to subclinical disease, rather than to clinical disease when beta-cell destruction is end-stage.