Our objective is to identify characteristics of β cells that survive immune attack. Our hypothesis is that
these residual cells express immune inhibitory molecules and/or decrease expression of diabetes
associated antigens. In addition, these cells may show changes consistent with dedifferentiated β cells.
Our studies of protein modifications have also shown that there are post-translational changes in
proteins produced by β cells during disease development. Finally, we have developed T cell library
assays that will enable us to identify novel antigens that may be found in islets during progression of
diabetes. Our objective is to determine whether β cells with these features can be found in the islets of
patients with T1D.
