Ann Diabetes Res | Volume 4, Issue 1 | Review Article | Open Access

Sertoli Cells and Complement Inhibitors: A Possible Mechanism to Increase Pancreatic Islet Viability

Rachel L Washburn¹, Gurvinder Kaur² and Jannette M Dufour^3*

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, USA

^*Correspondance to: Jannette M Dufour 

Abstract

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.

Keywords:

Islet transplantation; Hyperacute rejection; Type I diabetes; Complement; Sertoli cells

Citation:

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..