The Institute of Zoonoses Make breakthroughs

in Innate Immunity Research

On August 20, Associate Professor Peng Qisheng from the Institute of Zoonoses, in cooperation with the University of Oklahoma and the Veterans Hospital in the United States, published a research paper in Science Signaling, a journal under Science:

A  Physical  Interaction  Between  the  Adaptor  Proteins  DOK3  and  DAP12  Is  Required  to  Inhibit Lipopolysaccharide Signaling in Macrophage （http://stke.sciencemag.org/cgi/content/abstract/sigtrans;6/289/ra72).

Research on the molecular mechanism of innate immune tolerance induced by low-dose LPS stimulation has always been a hot and challenging issue in immunological research. Existing studies have shown that innate immune tolerance is regulated by the immunoglobulin family receptor TREM2 and the aptamer molecule DAP12, but the specific molecular mechanism remains unknown.

In this paper, by obtaining DOK3 knockout mouse peritoneal macrophages and bone marrow-derived macrophages, detecting the inflammatory response of low-dose LPS to macrophages, and studying the signal transduction pathway in phages of DOK3 on low-dose LPS stimulation through cell biology and molecular biology.

Studies have shown that TREM2 and DAP12 regulate natural immune tolerance through the DOK3 protein. This research provides a potential target for the treatment of immune tolerance-related diseases, and at the same time, it has conducted an in-depth study of the low-dose LPS stimulation caused by macrophage natural immune tolerance. The discussion enriches the mechanism of LPS immune tolerance, and advances the research of immune tolerance a big step forward.  

This research was funded by the Research Startup Fund of the Department of Agriculture of Jilin University.