In eukaryotes, in addition to TOLL-like receptors that can recognize viral RNA invading the body, in recent years, another cytoplasmic receptor RIG-I that can recognize viral RNA has been discovered. RIG-I can recognize the double-stranded RNA components of various RNA viruses such as hepatitis C virus (HCV) virus, and transmits signals through its own CARD and CARD of downstream signaling molecule MAVS to activate cell transcription The factors IRF-3 and NF-κB allow them to enter the nucleus and induce the expression of antiviral interferon, thereby initiating the innate immune response and regulating the subsequent acquired immune response, enhancing the body's ability to resist viral infections.

Under the guidance of mentor Ge Baoxue, a doctoral student from the Institute of Health Sciences, Shanghai Academy of Life Sciences and Shanghai Jiao Tong University School of Medicine, Chinese Academy of Sciences, found that stimulating peripheral macrophages with LPS (a major component of bacterial infection) can induce RIG -Expression of I. In macrophages and 293 cells, RIG-I interacts and co-localizes with the cytoskeletal protein Actin. Specific siRNA "knock-down" RIG-I or gene knock-out RIG-I reduces macrophage phagocytosis of bacteria. In addition, the RIG-I gene knockout mice were significantly more sensitive to bacterial infection than normal mice. The results of this study indicate that RIG-I is a very important regulatory molecule for the host to resist bacterial infections.

This research work was published in "Cell Host & Microbe" in August 2009. The research work was supported by the National Natural Science Foundation of China, the Ministry of Science and Technology 973 and the Ministry of Health major projects.

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