动物实验,小鼠模型 z-bo 2020-08-31 432

　　Previous reports have shown that the innate immune cells of non-obese diabetic mice are defective, and the Toll-like receptor TLR4 plays a role in preventing type I diabetes. Williamidgway, chair of the Department of Immunology, Allergy and Rheumatology at the University of Cincinnati, said his research team used the monoclonal antibody UT18 to enhance TLR4 activity and help people with new diabetes develop diabetes.

　　It is said to have overthrown the most. Diabetes is a recent development in obese mice. \r\n Satokiin: "Our research shows that certain molecules that use antibodies to stimulate the innate immune system can cause new diabetes in mice that already have diabetic symptoms. It can be reversed and has a high success rate because The beta cells in the pancreas are preserved in autoimmune attacks. This is the reason for the success of the reversal. The secret to reversing diabetes is usually to stop the onset in a short time. He said that the body’s onset takes a long time, but from a new onset to type I diabetes The time is still relatively short.\nThe research team of Yan Xiyun, Chinese Institute of Biophysics, Chinese Academy of Sciences, and Professor Liu Zhihua of the Center for Infection and Immunity, revealed the role of endothelial cell membrane receptor CD146 in inflammatory bowel disease and colorectal tumors .

　　Marked as an article on continuing medical education by the American Journal of Pathology (articles aiming to provide important and latest research progress in related fields), and specially published a comment entitled AdhesionMoleculeShowsPromiseforTreatingColitis. It is In recent years, experimental evidence has increasingly supported the idea that chronic inflammation causes tumors. There is a type of chronic inflammatory bowel disease, including ulcerative colitis and Crohn’s disease, which is a long-term recurrent bowel disease. Patients may have Colorectal tumors and abdominal pain and diarrhea. Although it is clinically known that CD146 expression in vascular endothelial cells is increased in inflammatory bowel disease, its mechanism and mechanism of action are still unknown. Yan Xiyun’s research team has long been involved in the structure and structure of endothelial cell membrane receptor CD146. Functional studies. In this study, they found that CD146 is an important nodular molecule connecting inflammatory bowel disease and colorectal tumors. The pro-inflammatory cytokines TNF? and IL1? activate the transcription of CD146, which directly upregulates the membrane of vascular endothelial cells The latter promotes the continuous development of chronic inflammation and the development of colorectal cancer by promoting the infiltration of inflammatory cells and angiogenesis. Through a series of animal model studies, including models related to ulcerative colitis and tumor models, When CD146 was specifically knocked out by vascular endothelial cells, the symptoms of inflammatory bowel disease mice were significantly reduced, and the infiltration of inflammatory cell water and new blood vessels was greatly reduced. More importantly, we found tumors with endothelial specific knockout of CD146 The model can significantly reduce the number of tumors and tumor volume. Based on the above findings, they used CD146-specific antibody AA98 to treat inflammatory bowel disease mice and ulcerative colitis-related tumor model mice, and significant therapeutic effects were observed , And effectively prevent tumors. Yes. This study not only describes the regulatory mechanism of endothelial cell CD146 in the transformation of chronic inflammation into cancer, but also provides new opportunities for the treatment of inflammatory bowel disease and the prevention of colorectal tumors related to it. Ideas and methods.

　　This work was supported by the National 973 Project and the National Natural Science Foundation of China.