Immunointervention studies with immunosuppressive drugs (Cyclosporin A
, Azathioprine) in type-1 diabetic patients after clinical diagnosis d
emonstrated that improvement of beta-cell function is not sufficient a
nd longlasting. Since 80-90% of the beta-cell mass are already destroy
ed at onset of type-1 diabetes, intervention studies with nicotinamide
and insulin (parenteral or oral) were undertaken in the early phase o
f type-1 diabetes. However, immunomodulation is restricted to familial
cases of type-1 diabetes (only 10% of all cases), since prediction of
the disease is not possible in the general population. It cannot be e
xcluded that the described immunintervention may only postpone but not
hinder the manifestation of type-1 diabetes. Interventions with toler
ance induction by BCG or GAD are promising, but did not yet result in
prevention of type-1 diabetes in humans. Finally, the most effective s
trategy would be primary prevention by vaccination or exposure prophyl
axis. Should type-1 diabetes prove to be a disease that is provoked th
rough molecular mimicry, i.e. an immunization by an environmental anti
gen, then strategies to avoid contact with the environmental trigger (
f.e. cow's milk protein) or to vaccinate against it (f.e. Coxsackie vi
rus protein PZ-c) could be adopted. If all these interventions are not
effective in the long term run, research should be concentrated on mo
lecular approaches after improvement in gene transfer technology.