She received Bachelor of Medicine degree from Peking University and obtained Ph.D. degree in immunology from Cornell University. She is currently Professor at Institute for Immunology, Tsinghua University and also serves as Vice Chair, Department of Basic Medical Sciences at Tsinghua University School of Medicine. Her research aims to better understand molecular mechanisms governing functionality of two key cell types involved in host defense and inflammatory responses, macrophages and intestinal epithelial cells (IECs) and to uncover transcriptional, translational and metabolic mechanisms that regulate macrophage and IEC responses to pathogenic and inflammatory cues. I have authored over 60 publications including corresponding-author research articles in journals such as Immunity, Nature Immunology, Cell Host & Microbe, Science Translational Medicine, Journal of Experimental Medicine, and Nature Communications. She is the recipient of multiple awards including Christina Fleischmann Award to Young Women Investigators from the International Cytokine Society, NSFC Distinguished Young Investigator Award, U.K. Royal Society Newton Advanced Fellowship and Young Scholar Award from Arthritis Foundation.  She also serve in editorial boards of journals including eLife, Science Advances and Protein & Cell and composed opinion/commentary articles for journals such as Immunity and Nature Immunology.

Defining monocyte heterogeneity in health and in rheumatoid arthritis patients

The Notch signaling pathway is conserved from Drosophila to mammals and is critically involved in developmental processes. Interestingly, the gene encoding the master transcription regulator of the Notch pathway, Rbpj, is among the rheumatoid arthritis risk loci yet the functional significance of Notch-RBP-J signaling in pathogenesis of rheumatoid arthritis is unclear. During the past several years, we and others have described a key regulatory role of the Notch pathway in innate immune and inflammatory responses. Notch1-RBP-J axis promotes inflammatory macrophage polarization while a Notch target gene Hes1 dampens inflammation by attenuating macrophage chemokine production. Importantly, in human rheumatoid arthritis patients, Notch target genes including Hes1 are highly expressed, which imposes heterogeneity on seemingly uniform monocyte populations. Expression of Notch target genes reversely correlates with monocyte inflammatory phenotypes. Such regulatory patterns impose positive and negative checkpoints on inflammatory responses and may have potential implications for pathogenesis and therapy of autoimmune and inflammatory disorders such as rheumatoid arthritis.

Key words: Monocyte, Notch, Rheumatoid arthritis