Bringing the bench to the bedside: Biology of Islet Cells
Anita Chong, Ph.D., Associate Professor (Transplantation) and Director of Transplantation Immunology Research, joined the faculty in 2002, and has already established a well-funded laboratory, with 2 R01s from NIH, as well as grants from the State of Illinois and Fujizawa. Her work addresses basic biological processes that are being extended to clinical practice.
Based on her work, clinicians hope to restore normal insulin production in Type I diabetes patients, without the need for long-term immunosuppressive therapy. Such work could benefit both pancreatic and islet transplantation patients. A key focus of her studies is to identify ways to alleviate both the alloimmune and ongoing autoimmune response in type I diabetic mice. She and her lab partners are in the process of identifying the alloreactive and autoreactive cells that mediate rejection pancreas or islet cells, and testing whether both pancreas and islet cells are equally amenable to tolerance induction.
In order to achieve a successful islet cell transplantation, cells must be both pure and viable. Dr. Chong’s work provides important knowledge of the life cycle and function of such cells, thereby supporting the work of Marc Garfinkel, M.D., Assistant Professor (Transplantation), who is involved in isolating and processing islet cells. She and her colleagues are directing studies of the ways to identify the optimal time from purification to transplantation of human islet cells into a mouse model.
They have already identified a number of strategies to blockade the immune cell function, thereby prolonging the allogeneic pancreas and islet cells in mice with Type I diabetes. Future studies will focus on enhancing the strategies that produce the tolerance and then translating these findings into the clinical settings.
Dengping Yin, M.D., Ph.D., Research Associate (Assistant Professor), preparing human islet cells for transplantation
A second area strives to improve engraftment and early function of islet grafts. Intraportal islet transplantation is associated with a high rate of deterioration of graft function in the early stages of transplantation – as many as 50-75% of islets fail to engraft in the liver following infusion into the portal vein. She and her colleagues have hypothesized that islets lodged in the portal vessels trigger a reduction of blood flow to the capillary bed, leading to localized portal vein thrombosis acute ischemia of the surrounding liver tissue and islets. By understanding how the early thrombotic and ischemic events induce early loss of islet graft function, they hope to develop clinical applications to enhance islet cell transplantation. |
|