Type 1 diabetes results from an autoimmune attack on the insulin-producing beta cells of the pancreas.  This autoimmune attack is driven primarily by T cells that mistakenly react to beta cell products.  The Serwold lab studies these T cells, in order to determine approaches to efficiently inactivate them in order to halt diabetes progression, or to enable beta cell transplantation.

We have recently shown that eliminating certain specific populations of autoimmune T cells can prevent diabetes in animal models.  We have engineered cytotoxic T cells to express novel, biomimetic chimeric antigen receptors that specifically kill certain autoimmune T cells, and have transplanted these engineered T cells into diabetes prone mice, and found that they confer protection to diabetes. We are using this novel approach to identify the key autoimmune T cell populations in type 1 diabetes, the timing of their activity and what stages they can be eliminated to prevent diabetes development. We are also optimizing and determining the therapeutic potential of this approach.

• Brown adipose tissue-derived MaR2 contributes to cold-induced resolution of inflammation
• Absence of CD11a Expression Identifies Embryonic Hematopoietic Stem Cell Precursors via Competitive Neonatal Transplantation Assay
• A biomimetic five-module chimeric antigen receptor (5MCAR) designed to target and eliminate antigen-specific T cells
• Increased β-cell proliferation before immune cell invasion prevents progression of type 1 diabetes
• Isolation of Highly Viable Thymic Epithelial Cells for Use in In Vitro and In Vivo Experiments
• Interleukin-17-Producing γδ T Cells Originate from SOX13+ Progenitors that Are Independent of γδTCR Signaling