UT Southwestern Biochemist and Breakthrough Award Winner Dr. Zhijian "James" Chen's most recent research is a long-standing question in national immunity.
Scientists have long wondered how a protein, NLRP3, can be stimulated to induce inflammation in front of a wide range of stimuli that are unrelated.
Dr. Chen, a professor of Molecular Biology and director of the UT Southwestern Center for Inflammation Research, received a 2019 Breakthrough Prize in Life Sciences to identify CGAS enzyme (GMP-AMP synthase cyclic). cells that respond to the cell's innate immune response.
Current study, posted today NatureDr. Chen has investigated another immune system that collects NLRP3 protein, that is, a complex of multiprotein complexes called inflammasomen. In front of curiosities with toxins and cholesterol crystals, inflammmasomes initiate paths to kill inflammatory cells, or pyrotesis Greek word pyro, meaning fire. Inflammomics produces the body's immune system, such as interleukins that help the body's immune response.
In addition, NLRP3 has highlighted the inflammation of the auto-inflammatory group of patients, including cryo-pyrhine-associated syndromes (CAPS), inflammatory inflammation syndrome (FCAS), gout, and inflammation of brain cells with Alzheimer's disease.
"This is a long question about how NLRP3 activists do not appear to have something like a chemical or structural similarity," said Dr. Chen, Howard Hughes Medical Institute Research, George L. MacGregor, Distinguished Biomedical Science Chair, and UT Southwestern Defense Defense Genetic Center teacher. "These findings make NLRP3 a new pathway to develop therapeutic-oriented treatment for inflammatory diseases."
Through a combination of biochemical, imaging and genetic approaches, PhD Chen and PhD PhD in Dr. Jueqi Chen, the main researcher and non-contact, found themselves previously unknown within cells.
Several stimuli are called the organoleptic trans Golgi network (TGN), to break giant vesicles or fluid filled bags. These Vesicles have a special lipid supplement (PI4P) that connects to a specific region NLRP3. This connection causes several events to trigger inflammatory activation.
"NLRP3 is the only inflammammary, caused by a large number of stimuli," said Dr. Chen. "This study does not directly recognize indifferent agents, because it detects structural changes caused by multiple operations caused by inflammammant NLRP3, which cause cell damage, because NLRP3 activation reminds the model of the plant to deal with plants & # 39; Several threats have been made when host targets have changed, which cause changes caused by pathogens.
"When connecting the Trans-Golgi network locks, as a" modified car ", NLRP3 binds potentially pathogens and dangerous molecules.