Rachel L Washburn1, Gurvinder Kaur2 and Jannette M Dufour3*
1Department of Immunology and Infectious Disease, Texas Tech University Health Sciences Center, USA 2Department of Medical Education, Cell Biology and Biochemistry, Texas Tech University Health Sciences Center, USA 3Department of Cell Biology and Biochemistry, Immunology and Infectious Disease and Medical Education, Texas Tech University Health Sciences Center, USAFulltext PDF
Type I Diabetes Mellitus (TIDM) is an autoimmune disease in which the immune system attacks and destroys the insulin producing β cells of the pancreatic islets. Insulin is an essential hormone released in response to elevated blood glucose levels, allowing the uptake and utilization of glucose by muscle and adipose tissue. The establishment of an immune privileged environment by Sertoli cells (SCs) through several mechanisms, including inhibition of complement mediated cell lysis by production of complement inhibitor proteins, may offer a unique alternative to prolong graft survival. Further understanding of how SCs use complement inhibition to incite immune protection could be translated into increasing the viability of pancreatic islet transplants.
Islet transplantation; Hyperacute rejection; Type I diabetes; Complement; Sertoli cells
Washburn RL, Kaur G, Dufour JM. Sertoli Cells and Complement Inhibitors: A Possible Mechanism to Increase Pancreatic Islet Viability. Ann Diabetes Res. 2020;4(1):1013..