Research Interests

The majority of our work is focused on type 1 autoimmune diabetes, which results from T cell mediated destruction of insulin producing beta cells in the pancreas.  Loss of beta cells leads to dysregulation of glucose metabolism and a life-long dependency on insulin injections. There is no cure for type 1 diabetes, and we still have limited understanding of the immunologic and metabolic dysfunction that ultimately leads to beta cell loss.

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Members of the laboratory utilize genetically modified mouse models, multi-color flow cytometry, high resolution and 2-photon live imaging, single cell transcriptomics and epigenetic profiling  to study autoimmune and regulatory T cell function. We are particularly interested in Foxp3+ regulatory T cells. Foxp3+ regulatory T cells employ multiple mechanisms to maintain immune and metabolic homeostasis, suppress autoimmunity, and aid in tissue repair. T cell receptor signaling is counter-balanced by cellular interactions with tissue cells and effector T cells to guide the development of Treg sub-populations with specialized functions. Current work in the lab is focused on how Tregs integrate T cell receptor signaling with tissue-derived cues to modulate their suppressive functional program. Additional projects are focused on transcriptional and epigenetic mechanisms associated with autoimmune T cell function, autoimmune T cell memory, and T cell exhaustion in chronic inflammation.

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Main areas of investigation: (1) Regulatory T cell function in autoimmunity, (2) TCR affinity, specificity and TCR activation of regulatory and effector T cells in autoimmunity, and (3) mechanisms of autoimmune T cell  persistence in autoimmunity.

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