Sanja Glisic, Ph.D. Assistant Professor, Pediatrics Specialization: Genetics Tel: (414) 456-4572 Dr. Glisic's CV Email Dr. Glisic
Type 1 Diabetes is a disease developed as a consequence of T-cell mediated destruction of insulin-producing beta-cells, resulting in life-long dependency on insulin. The disease has strong genetic component, although environmental contribution has to be acknowledged. We are interested in the role T-cells have in T1D pathogenesis. Although there are several subsets of T cells, we are mostly interested in T cells with regulatory properties (CD4+CD25+high T cells or natural Tregs).
Isolation of natural Treg cells is still subject of many studies, as the unique surface marker has yet to be found. We are currently combining proteomics with immunogenetics in a search for a better marker. Using a specific apoptosis stain combination developed in our lab, we were able to detect increased Treg apoptosis in recent-onset T1D subjects (recruited within first 8 months from the diagnosis) and in multiple autoantibody-positive unaffected subjects, compared to the rest of T1D –relevant subject groups.
We have also detected increased Treg apoptosis in subjects with high HLA risk, possessing T1D susceptible HLA DR*04-DQB1*0302 and HLA DR*03-DQB1*0201 haplotypes, compared to low risk HLA haplotypes. How long before the onset does Treg apoptosis start? Is increased Tregs apoptosis marker for T1D? Can it serve as a screening tool for detection of prediabetic individuals? Can increased Treg apoptosis help predict existence/cessation of the honeymoon period? Why Tregs apoptosis happens and what is causing their death? Why don’t other T cell subsets die by apoptosis?
Studies exploring this phenomenon and answering posed questions are on the way.
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