Rate My Professor Shoutang Wang

Shoutang Wang is an Assistant Professor in the School of Biomedical Sciences at the University of Hong Kong, part of the Faculty of Medicine, where he established his own laboratory in 2023. He earned his BS from Jilin Agricultural University, MS from Jilin University, and PhD from University of Paris-Saclay in 2017 at the Institute Gustave-Roussy in France, with training in developmental hematopoiesis of the myeloid lineage. Following his PhD, he joined Professor Marco Colonna’s laboratory at Washington University School of Medicine in St. Louis, USA, for postdoctoral training, contributing to projects on TREM2 functions in microglia in mouse models of Alzheimer’s disease.

Wang’s laboratory focuses on interactions between the immune system and the central nervous system during neurodegenerative diseases such as Alzheimer’s disease, to understand disease development and progression and explore potential treatments. His research interests include microglia and neurodegenerative diseases, immunotherapy and translational medicine, and cell signaling. He received the 2017 Keystone Symposia Future of Science Fund scholarship. Key publications as first or corresponding author include: Wang, S., and Colonna, M. (2023). The microglial immunoreceptor tyrosine-based motif-Syk signaling pathway is a promising target of immunotherapy for Alzheimer’s disease. Clinical and Translational Medicine 13, 10-13; Wang, S., et al. (2022). TREM2 drives microglia response to amyloid-β via SYK-dependent and -independent pathways. Cell 185, 4153-4169.e19; Wang, S., et al. (2020). Anti-human TREM2 induces microglia proliferation and reduces pathology in an Alzheimer’s disease model. Journal of Experimental Medicine 217; Wang, S., and Colonna, M. (2019). Microglia in Alzheimer’s disease: A target for immunotherapy. Journal of Leukocyte Biology 106; Wang, S., et al. (2021). Lyl-1 regulates primitive macrophages and microglia development. Communications Biology 4, 1382; Ellwanger, D.C., et al. (2021). Prior activation state shapes the microglia response to antihuman TREM2 in a mouse model of Alzheimer’s disease. Proceedings of the National Academy of Sciences 118.