As an important part of natural immunity, NLRP3 inflammasome plays an important role in the development of immune response and disease, and its overactivation can lead to a variety of major human diseases such as alzheimer's disease, inflammatory bowel disease, diabetes and malignancy. Previous studies have found that the Danger signal molecules(Danger Signals) induced mitochondrial damage that leading to excessive activation of NLRP3, but the detailed regulation mechanism that how does the body maintains mitochondrial homeostasis to prevent excessive activation of NLRP3 is rarely reported. Professor Xu Qiang and professor Sun Yang research team's latest work found that protein tyrosine phosphatase SHP2 can be transferred to the mitochondria by the NLRP3 activator ATP, the crystallization of uric acid and the bacteriocin in the NLRP3. In the mitochondrial outer membrane protein Tom20 / Tim23 Tom40 complexes and mitochondrial membrane protein complexes, SHP2 quickly through the outer and inner membrane targeting mitochondrial matrix, combined with mitochondrial membrane protein ANT1, remove its 191 tyrosine phosphorylation, and stability of mitochondrial membrane potential, inhibition of mitochondrial DNA, and the release of reactive oxygen species, cut the resulting excessive activation of NLRP3 inflammatory corpuscle.

       The work found an important endogenous fine regulation of NLRP3 inflammatory small body activation new mechanism - activating negative regulation signal to maintain mitochondrial homeostasis shortly after inflammatory response. A negative regulatory mechanism to clarify will help us understand how the body is fine regulation of inflammatory response so as to maintain a stable internal environment, as well as inflammation related provides a new way of thinking and solving strategy for disease control and prevention.