Project Description

Type 1 diabetes (T1D) is an autoimmune disease in which the immune system destroys insulin-producing cells (beta cells) in the pancreas, reducing insulin levels and leading to high blood glucose. Regulatory T (Treg) cells are immune cells that help the body recognize itself; they prevent autoimmune diseases, including T1D.

mTORC1 is a protein complex that functions as a nutrient sensor and controls protein synthesis. mTORC1 regulates Treg cell development, number and function. In addition, mTORC1 activation of one of its targets (4E-BP2) increases the number of beta cells. More importantly, beta cells lacking 4E-BP2 are resistant to treatment with cytokines – immune proteins that can cause cell death. However, the extent to which 4E-BP2 deletion prevents type 1 diabetes development in mice is unclear.

Since the mTORC1/4E-BP2 pathway has beneficial effects on beta cells and helps control Treg cell number and function, we hypothesize that it could be involved in T1D prevention by increasing beta-cell survival and regulating autoimmunity. This project could lead to novel T1D therapies targeting the two major components in the development of T1D: autoimmune response and beta-cell survival.

To assess this hypothesis, we have assembled a multidisciplinary research group composed of researchers with expertise in beta cell biology, intracellular signaling, diabetes, and immunology.

Click HERE to view Dr. Pecanha’s video.