I型糖尿病 z-bo 2020-10-08 307

　　Type 1 diabetes occurs when the human immune system destroys the beta cells in the pancreas that produce insulin. In recent years, scientists have learned how to grow a large number of replacement beta cells, but researchers are still trying many methods to protect these cells from immune attack. Recently, researchers at the Joslyn Diabetes Center have discovered new methods that can ultimately help protect these transplanted beta cells and delay the onset of the disease. Stephen Kistler, an associate professor at Harvard Medical School, said in a study on mouse models and human cells that he will enhance beta cell resistance by targeting a protein called "reninase" Power to protect yourself from the immune system. Said yes.

　　First, the authors used CRISPR gene editing-based screening technology to simulate type 1 diabetes using β cell lines from "non-obese diabetic" (NOD) mice. "We hope that genome CRISPR screening is a powerful tool for discovering new targets and will help us find mutations that protect beta cells," said co-author Yi. Through CRISPR's screening of surviving β cells, the authors obtained more than 12 genes of interest. The most striking is the renal enzyme gene associated with type 1 diabetes in previous studies.

　　Next, the researchers created NOD mouse β cells, some of which "knocked out" kidney enzyme genes. They transplanted these cells into NOD mice with autoimmune diabetes. The results showed that wild-type β cells eventually died after transplantation, while kidney enzyme knockout cells survived. Later, the researchers began to study whether cells lacking the kidney enzyme gene caused a weakened pancreatic T cell response. Scientists have found that compared with normal beta cells, T cells are less likely to attack these knockout cells.