Maternal immunity to insulin does not affect diabetes risk in progeny of non obese diabetic mice.

It has been suggested that maternal environment, in particular maternal autoantibodies, modify the risk of developing autoimmune diabetes in offspring. The aim of this study was to determine whether modification of maternal environment and maternal diabetes risk through immunization affects autoimmune diabetes risk in the progeny. The risk of developing insulin antibodies and of developing diabetes was determined in 113 female progeny of non obese diabetic (NOD) dams that were immunized with insulin, control antigen or vehicle before or during pregnancy. Although NOD dams immunized with insulin were rendered diabetes resistant (40% diabetes by age 36 weeks versus 100% in control dams), diabetes development in their female offspring (72%, 26/36) was similar to that in female offspring of dams immunized with glucagon (82%, 22/27) or vehicle (76%, 19/25). Furthermore, no significant differences in diabetes development or insulin autoantibody titres were observed between female progeny of insulin autoantibody positive NOD dams (82% diabetes by age 36 weeks, 18/22), insulin autoantibody negative NOD dams (75%, 41/55), and NOD dams that had antibodies against exogneous insulin (71%, 22/31). The findings suggest that modification of the maternal risk for autoimmune diabetes via antigen-specific immunization is not transferred to progeny and that fetal exposure to insulin autoantibodies does not increase the risk for diabetes development.