Matthew Wai Heng Chung
Academic and Work Experience Prior to Sept 2019 Programme Start
I obtained my bachelor’s degree in Biomedical Sciences and MPhil in Structural Biology at the University of Hong Kong. I completed an MSc in Health Data Science at University College London.
PhD Programme – Year 1 – MRes and Project Rotations
During the first year of the programme I completed three rotations all related to the digestive system:
Intestinal organoids response to type 3 innate lymphoid cell cytokines – Dr Joana Neves and Dr Rocio Martinez-Nunez.
Pancreas development and the contribution of epithelial-mesenchymal interaction informed by single-cell RNA sequencing – Dr Francesca Spagnoli and Dr Alessandra Vigilante.
Liver regeneration pathway discovery using network bioinformatics to integrate single-cell transcriptome and interactome databases – Dr Tamir Rashid, Prof Francesco Dazzi, with generous help from Prof Franca Fraternali during the UK COVID-19 lockdown.
PhD Programme – Years 2 to 4 – Doctoral Studies
I will be working with Dr Subhankar Mukhopadhyay and Prof Alberto Sanchez-Fueyo to study macrophages. Macrophage is a key cell type in the innate immune system that is ubiquitously distributed in almost every tissue and organ of the body and carries out a variety of homeostatic and immune functions. A balance between macrophage activation, regulation and its reparative function is critical to restoring tissue homeostasis without compromising host defence.
Excessive macrophage activation contributes to many inflammatory diseases including inflammatory bowel disease (IBD) and non-alcoholic fatty liver disease (NAFLD). Thus, resetting the optimal balance of macrophage activation is an attractive therapeutic strategy to prevent or treat organ-specific inflammatory diseases. During my PhD, I will use human iPSC-derived macrophages to investigate how they become activated after tissue damage, particularly through scavenger receptors in collaboration with other pattern recognition receptors.
I will also study how the IL-10/PGE2 axis and regulatory T cells limit macrophage activation, which will be validated in a mouse liver injury model. A full understanding of these mechanisms will guide the development of potential therapeutic targets that harness specific macrophage properties for clinical benefit.
