Zhang, Shirley
Shirley is in the Molecular and Medical Pharmacology Graduate Program, and joined the CMB Training Program in 2022.
Mentor: Dr. Maureen Su
Type I diabetes (T1D) is an autoimmune disease caused by T-cell mediated destruction of beta-cells, which produce insulin in the pancreatic islets. T1D is the most prevalent form of diabetes amongst children and affects more than 500K children worldwide. The rapid rise in T1D incidence between 2002 and 2015 is too fast to be attributed to genetic factors alone. More likely, this rapid rise may reflect environment-influenced epigenetic regulation, particularly in T cells. A recent clinical trial studying the effect of an anti-CD3 drug on T1D prevention shows the correlation between decreasing lymphocytes and lowered T1D risk amongst the relatives of T1D patients, highlighting the importance of T cells for human T1D. However, the identity of key epigenetic regulators that control diabetogenic T cells is unclear. Our previous study shows a critical role for the epigenetic regulator UTX in CD4+ T cell differentiation during chronic virus infection, demonstrating UTX’s role in modulating T cell activity. To study T1D, we developed a mouse model with UTX deficiency in T cells and discovered that UTX deficiency protects mice from T1D. Currently, we are studying the molecular mechanism of protection from T1D using this mouse model with UTX deficiency in T cells.
