Two army great amynologic basic research makes the new development
It is reported ' The reporter reporter Xiao Xin and Xing YuanXiang) Go through 10 to tackle key problems in academician's laboratory of amynologic great wave of research institute Cao Xue of the second army medical university in Shanghai, find independently a new kind of is suffused with usually melting enzyme Nrdp1, can promote macrophages and the tree to dash for ward form cells etc. through the alternative, produce interferon of Model me and inhibit the inflammation cell factor from producing, thus help the organism to remove the virus to is infected with and weakens inflammation to damage effectively. Have issued this research results in a new " natural immunology " published. Organism immune system, after discerning invasion of the virus, how start effective immunity, reply, react so as to resist the virus, infect? How to control inflammation followed to react while removing virus, thus make the organism remove the virus and does not damage the normal tissue effectively? Which important immune cells and immune molecule participate in this immunity discerning and immune regulating process? This is the great science question that the international immune educational circles are paid much attention to for a long time. Cao XueTao laboratory first cloned a new molecule while dashing for ward the genetic library of form cell independently from people's tree in 1998, found this molecule related to cell death and named it as at that time " The death resists albumens " . 3 years later, the foreign scholar reported the little mouse homology molecule of this molecule successively, name it as several names such as Nrdp1, and prove it and tumour cells one withers and dying to relate to forming mechanism of tumour. Cao XueTao academician and Wang Chen Dr., great wave Chen well up seminar that associate professor,etc. make up, explore the new immunological function of this molecule actively. Discover, molecule this suffused with, take usually as a new kind of enzyme can combine in immunity discerning with two the intersection of signal and member (MyD88 and TBK1)s that play an important role under immune adjustment directly ,What clicked and lay between leading was suffused with the course of usually melting and promote MyD88 to degrade and activate TBK1 through different location, thus inhibit the intersection of MyD88 and the intersection of signal and thorough fare touch off inflammation of macrophage,etc. but the intersection of cell and production of factor promote the intersection of TBK1 and the intersection of signal and the intersection of Model I and production of interferon that thorough fare touch off. Researchers pass the vivo experimentation of little mouse of the transgenosis, prove Nrdp1 can inhibit the inflammation cell factor from producing through the fact that the alternative promote the virus to infect Model I interferon induced to produce, thus help the organism to remove the virus to is infected with and weakens inflammation to damage effectively. It is reported, this research has offered the new target for the fact that new medicine which treated inflammation disease is designed.
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