Department of Immunology, Cleveland Clinic Foundation
Dr. Xiaoxia Li received her Bachelor degree from Wuhan University in China and came to the United States for her doctoral training in 1983. She received a Ph.D. in Biochemistry, Molecular and Cell Biology from M.D. Anderson Cancer Center, University of Texas. She did post-doctoral training in Biochemistry and Molecular Biology with Dr. George Stark at the Cleveland Clinic, where she joined the Department of Immunology as Assistant Professor in 2001.
She is currently a Full Professor in the in the Lerner Research Institute and Professor of Molecular Medicine at Cleveland Clinic Lerner College of Medicine. Dr. Li has authored over 100 peer-reviewed papers. During the last several years, the discoveries from her laboratory have illustrated many of the intricate and complex pathways that control innate and adaptive immunity. Her lab elucidated important signaling mechanisms governing how IL-1R-TLRs trigger the inflammatory response by coupling NFkB activation with posttranscriptional pathways to induce robust production of cytokines and chemokines. These studies provide significant insight into fundamental mechanisms regulating innate immunity and yield essential information for the selection of potential drug targets. In addition, her laboratory was one of two groups that discovered SIGIRR, a member of the TLR family that provides negative regulatory function. This finding was extended to show that SIGIRR modulates intestinal inflammation/tumorigenesis by maintaining the microbial tolerance of the colonic epithelium and limiting the development of pathogenic Th17 cells.
The study of SIGIRR provides a novel mechanism by which the mucosal surface responds to commensal flora and participates in innate and adaptive immune responses. Finally, Dr Li’s laboratory was one of the groups that identified Act1 as a necessary signaling component in the IL-17 pathway. Using this she has made important contributions to understanding the molecular and cellular mechanisms that regulate the functions of IL-17 in vivo. For example, a variant of Act1 (D10N) has been linked to psoriasis susceptibility in humans and Dr. Li’s laboratory has demonstrated that this molecular form is defective in its interaction with the molecular chaperone Hsp90, resulting in a global loss of function of Act1. This work thus demonstrates the molecular basis for the contribution of Act1 (D10N) in psoriasis and psoriatic arthritis.
Dr. Li is recognized for her discovery of novel genes implicated in immune signaling pathways.