Scientific research shows that once pathogenic pathogenic microorganisms such as viruses and bacteria invade the body, the immune system will quickly initiate an anti-infective immune response. But the question that has plagued the immunology community for a long time is what kind of cellular and molecular mechanisms the body's immune system uses to distinguish between "self" and "non-self", so as to specifically perceive the invasion of exogenous pathogenic microorganisms and how to effectively start immunity Response effect to kill and remove pathogenic microorganisms. In October last year, Cao Xuetao was invited by Nature-Immunology to write a review of the molecular mechanisms by which immune cells recognize the DNA of pathogenic microorganisms to induce the production of type I interferon, and proposed six research hotspots in the field.
The Lrrfip1 discovered this time can directly recognize and bind the double-stranded DNA and double-stranded RNA of the pathogenic microorganism, and then bind and activate a signaling molecule, and then bind to the key transcription factor produced by type I interferon to promote the interference of acetyltransferase P300. The promoter region of interferon aggregates to form an interferon gene expression enhancing three-phase complex, thereby promoting interferon production. The study found a new molecular pathway that is different from the classical model, consisting of intracellular nucleic acid recognition molecule Lrrfip1 and its downstream signaling molecules, immune recognition pathogenic microorganism nucleic acids, and triggers the production of type I interferon, which provides the design of anti-infective drugs. New targets and ideas.
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