Type 1 diabetes (T1D) is one of the most common chronic diseases of childhood with onset peaking between 5-7 years of age and around puberty. Early childhood-onset T1D often exhibits severe beta-cell depletion compared to late adult onset T1D. We propose to test the hypothesis that immature beta-cells in early childhood are more susceptible to autoimmune destruction, whereas the cell death of mature beta-cells in adult onset T1D undergoes different kinetics and its process is substantially slower than previously considered. A better understanding of distinct beta-cell destruction and preservation during childhood could lead to new therapeutic strategies to treat young children with T1D.
