Major
Biology
Research Abstract
Type 1 diabetes (T1D) is an autoimmune disease that affects millions of children and adults worldwide. In this disease, white blood cells (Leukocytes) invade, attack, and destroy the Islets of Langerhans in the pancreas, resulting in increased blood glucose levels. Patients with T1D must use exogenous insulin injections, which can lead to many side effects over the lifespan of the person. Therefore, understanding the pathogenesis of this disease is crucial to develop new treatments for patients. The non-obese diabetic (NOD) mouse is a rodent model of T1D as well as other autoimmune diseases such as Sjogren’s syndrome, where immune cells attack the salivary glands. In this study, we compared diseased and healthy tissues in the NOD mouse (Wild Type: WT) as well as mice lacking TGFβ signaling in the regulatory T (Treg) cell lineage (Flox mice). Treg cells are specialized CD4+ T cells, whose function is to suppress effector cells and maintain self-tolerance. Interestingly, the Flox mice do not develop diabetes but do develop a different autoimmune disease: peripheral neuropathy, a condition in which the peripheral nerves are damaged. These mice rapidly lose all function in their limbs and suffer from severe weight loss. We were interested in determining if these mice had any additional sites of autoimmune inflammation. We characterized multiple tissues using histological analysis, including islets, nerves, salivary glands, thyroid, small intestine, kidney, and others. Together, this data will identify additional organs that may be either damaged or protected from disease in Flox animals and contribute to our understanding of how TGFβ signaling in Tregs influences their function in NOD mice.
Faculty Mentor/Advisor
Allyson Spence
Included in
Torn Between two Diseases: Changes in TGFβ Signaling Prevents Diabetes but Promotes Neuropathy
Type 1 diabetes (T1D) is an autoimmune disease that affects millions of children and adults worldwide. In this disease, white blood cells (Leukocytes) invade, attack, and destroy the Islets of Langerhans in the pancreas, resulting in increased blood glucose levels. Patients with T1D must use exogenous insulin injections, which can lead to many side effects over the lifespan of the person. Therefore, understanding the pathogenesis of this disease is crucial to develop new treatments for patients. The non-obese diabetic (NOD) mouse is a rodent model of T1D as well as other autoimmune diseases such as Sjogren’s syndrome, where immune cells attack the salivary glands. In this study, we compared diseased and healthy tissues in the NOD mouse (Wild Type: WT) as well as mice lacking TGFβ signaling in the regulatory T (Treg) cell lineage (Flox mice). Treg cells are specialized CD4+ T cells, whose function is to suppress effector cells and maintain self-tolerance. Interestingly, the Flox mice do not develop diabetes but do develop a different autoimmune disease: peripheral neuropathy, a condition in which the peripheral nerves are damaged. These mice rapidly lose all function in their limbs and suffer from severe weight loss. We were interested in determining if these mice had any additional sites of autoimmune inflammation. We characterized multiple tissues using histological analysis, including islets, nerves, salivary glands, thyroid, small intestine, kidney, and others. Together, this data will identify additional organs that may be either damaged or protected from disease in Flox animals and contribute to our understanding of how TGFβ signaling in Tregs influences their function in NOD mice.
