DETROIT Collaborating with researchers from the Northwestern University Feinberg School of Medicine in Chicago, a research team at Wayne State University's School of Medicine led by Kezhong Zhang, Ph.D., has contributed to an important discovery in the inflammatory stress mechanism and specific inhibitor for the treatment of rheumatoid arthritis.
The team led by Zhang, associate professor of immunology and microbiology and Wayne State's Center for Molecular Medicine and Genetics, and the team led by Deyu Fang, Ph.D., associate professor of pathology at Northwestern University Feinberg School of Medicine, worked together to discover the key inflammatory stress response that drives the development of rheumatoid arthritis. Their studies revealed that inflammatory stimuli trigger cell surface toll-like receptors of macrophages, the white blood cells that subsequently activate the Unfolded Protein Response transducer IRE1a to promote arthritis syndrome in the tissues around the joints.
Their work identified a specific IRE1a inhibitor that can efficiently prevent arthritis in animal models.
The study, "Toll-like receptor-mediated IRE1a activation as a therapeutic target for inflammatory arthritis," was published in the prestigious scientific journal EMBO. Zhang served as a corresponding author. The study can be read at http://www.nature.com/emboj/journal/v32/n18/full/emboj2013183a.html.
"This is a notable work in the understanding of the stress mechanism for the development of rheumatoid arthritis," Zhang said. "For the first time, we revealed the molecular targets of Unfolded Protein Response and Toll-like Receptor signaling and their interaction mechanism in the progression of inflammatory arthritis. Our study not only identified previously unknown molecular targets, but also pointed out a specific inhibitor that can efficien
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Wayne State University - Office of the Vice President for Research