Feedback immune autoi recognition promotes inflammation receding in a timely manner

April 26, 2018,
published a research paper by Cao Xuetao, a member of the Chinese Academy of Engineering, former president of the Chinese Academy of Medical Sciences and president of Nankai University, reporting on the team's new breakthrough in the field of natural immunity and inflammation control research, and proposing a new mechanism and new viewpoint for self-immune identification to trigger anti-inflammatory effects and prevent antiviral natural immune over-response in a timely manner, thus maintaining the body's self-stabilization.
function of immunity is to recognize the invasion of "non-I" pathogens and activate the natural immune response, protect the "self" body, maintain their own stability. Once the infection is controlled, the natural immune response needs to be terminated in time, otherwise it will cause the body's own inflammatory damage, therefore, how to effectively and moderately respond to anti-infection natural immunity and timely termination has been the basic scientific problem in immunology research.
With the support of the Medical and Health Science and Technology Innovation Project of the Chinese Academy of Medical Sciences and the Project of the Basic Science Center of the National Fund Committee, Cao Xuetao and Jiang Minghong, a professor in the Department of Immunology of the Institute of Basic Medicine of the Chinese Academy of Medical Sciences, and Zhang Shikun, a doctoral student, conducted a study on whether the late virally infected body would produce a new molecule of self-protective anti-inflammatory inflammation, and conducted research around RIG-I, a natural immunological body that recognizes viral RNA, and over a period of six years found ING-I from viral infection macrophages. The exact binding point between lnc-Lsm3b and RIG-I can be determined by the cross-link immunoseccumulation (iCLIP) technique of single nucleotide accuracy, which can be combined with several long-chain non-coding RNA (lnc-RNA), which is named lnc-Lsm3b, which significantly induces the generation and selective binding of RIG-I protein molecules in the advanced stages of antiviral response. It was then found that lnc-Lsm3b was able to make RIG-I no longer bind to viral RNA through the "molecular bait" competition mechanism, so that RIG-I was in an inactive state, thus reciprocizing the natural immune response and avoiding excessive inflammation.
the study suggests that the body's own RNA can be "self-identifying" way feedback timely termination of the "non-I" recognition triggered by the natural immune response and inflammatory response, to achieve the body's self-protection, self-stabilization. The discovery of the new RNA molecule lnc-Lsm3b and the new mechanism for self-immune identification to promote inflammation receding can provide new ideas for the prevention and treatment of inflammatory diseases. (Source: Science.com)