Dr. Kathy Lui is currently an Associate Professor at the Department of Chemical Pathology, The Chinese University of Hong Kong. She received her Ph.D. degree in Immunology from University of Oxford U.K. in 2009. After that, she had her postdoctoral training at Harvard University, U.S.A until 2014. Her postdoctoral work focused on deciphering the therapeutic potential of the first-in-human modified mRNA (i.e. VEGF modRNA) that has been now undergoing phase-II clinical trial by Moderna and AstraZeneca in patients receiving coronary bypass surgery. In 2014, she started her own laboratory and focused to understand the immunoregulation of cardiovascular diseases and repair. She has published over 90 peer-reviewed articles and received numerous awards and honors including the Croucher Innovation Award in 2017, founding member of the Young Academy of Sciences of Hong Kong in 2018, the first batch of NSFC Excellent Young Scientists in Macau & Hong Kong in 2019, and the RGC Research Fellowship in 2022. Dr Lui has been an early career editorial board of Circulation Research (American Heart Association) in 2020-2022, and an editorial member of Cardiovascular Research (European Society of Cardiology). She is also the current Chairperson of the Hong Kong Society for Immunology.
Accumulating evidence has demonstrated that immune cells such as macrophages play an important role in regulating the progression of cardiovascular disease and repair. After injury, danger signals released by the damaged tissues trigger the initial pro-inflammatory phase essential for removing cellular debris that is later replaced by the anti-inflammatory phase responsible for tissue healing. Impaired immune regulation can lead to excessive scarring and fibrosis that are detrimental for the restoration of tissue function. Our earlier work has shown that regulatory T-cells respond to cardiovascular injury that are indispensable for the repair and regeneration of the cardiovascular system. In this talk, we will summarize the roles of several T cell subsets not limited to their direct effect on polarizing macrophages after injury, but also their direct function in enhancing replication of cardiovascular cells during tissue repair and regeneration. We will also demonstrate the possible molecular mechanisms by which T cells mediate the development of cardiovascular diseases such as myocardial infarction, ischemia and atherosclerosis through regulating the transcriptomic and epitranscriptomic events in cardiovascular cells. Altogether, our findings may suggest some clinically relevant insights into the development of therapeutics targeting T cells in cardiovascular repair and regeneration.