Medical

State Key Laboratory of Immunology, Shanghai Second Military Medical Institute Immunologic Cao Xuetao big Academy of Sciences Laboratory for 10 years after discovery of a new type of enzyme ubiquitin Nrdp1, through the selective promotion of macrophages and dendritic cells produce I-type interferon, inhibit inflammatory cytokine production, help the body clear the infection effectively reduced inflammation and damage, and thus knowledge of the immune cells to resist viral infection and control inflammation of the new molecular mechanisms of immune regulation. The newly published "Nature Immunology" magazine published the results of the new.

immune system in the identification of viruses, how to activate an effective immune response against HIV infection? How to clear the virus while in the control of inflammatory response associated with the body can effectively clear the virus does not damage normal tissues? What are the important immune cells and immune molecules involved in the immune recognition and immune regulation process? This is a long-standing international immunization of great concern to the academic major scientific problems.

Cao Xuetao laboratory in 1998 from human dendritic cells gene library in the first cloning of a new type of independent elements, at that time found that the molecular and cell death, and named as the death of the resistance protein. 3 years after the foreign scholars who have reported the molecular homology of the mouse, named several Nrdp1 name, and proved it with tumor cell apoptosis and tumor formation mechanism. Cao Xuetao academicians and Dr. Wang Chen, Yong Chen, associate professor of research, such as the composition of the group found that the molecule of ubiquitin as a new enzyme, direct binding to the immune recognition and immune regulation plays an important role in the two signaling molecules ( MyD88 and TBK1). Through different sites of ubiquitin-mediated process is to promote the degradation of MyD88 activated TBK1, thereby inhibiting the MyD88 signaling pathway triggered by macrophages and other inflammatory cytokine production, and promote the TBK1 signaling pathway triggered by IFN-I produced. Transgenic mice through in vivo experiments demonstrated selective Nrdp1 can promote HIV-I by interferon-induced, while inhibiting inflammatory cytokine production, help the body clear the infection effectively reduced inflammation and damage.