Date: Friday, 13 May 2022

Time: 5:00 p.m. - 6:00 p.m.

Venue: Cheung Kung Hai Lecture Theatre 1, G/F, William M.W. Mong Block, 21 Sassoon Road, Pokfulam, Hong Kong

5:00 p.m.

Presenter: Mr. Nickolas Jia Ming TEO, PhD candidate
Primary Supervisor: Dr. Heidi Guang Sheng LING
Presentation Title: The role of granulocytic myeloid-derived suppressor cells in tumour-immune co-evolution
Abstract: The immune response to cancer is a critical aspect of the tumour microenvironment (TME), as it influences cancer development and drives intratumoural heterogeneity. Previously research has well-established the role of the adaptive immune system for tumour development, particularly T cells, which exert strong selective pressures on the tumour. They drive the development of tumour clones capable of escaping immunosurveillance. However, the role of the innate immune system in shaping cancer evolution is much less understood. The current project aims to address this knowledge gap by positing a novel reciprocal communication axis between granulocytic myeloid derived suppressor cells (gMDSCs) and cancer stem cells (CSCs). Our data suggests that CD133⁺ CSCs promote gMDSC development in the TME, who in turn downregulate the antigen presentation machinery of CD133⁺ CSCs, thereby facilitating their immune evasion.

5:30 p.m.

Presenter: Miss Bei WANG, PhD candidate
Primary Supervisor: Dr. Alan Siu Lun WONG
Presentation Title: Genome-wide CRISPR screening for identifying host factors essential to SARS-CoV-2 Spike-mediated syncytia
Abstract: The presence of infected multinucleated syncytial pneumocytes is a typical characteristic in severe cases of COVID-19. The formation of syncytia is believed to contribute to the disease pathology by facilitating viral transmission, immune evasion, and inflammatory response. Studies have demonstrated that infected host cells expressing the SARS-CoV-2 Spike protein can fuse with neighboring ACE2-expressing cells and form syncytia. Identifying host factors crucial for syncytia formation may reveal new therapeutic targets. It is reported that Spike/ACE2-mediated cell fusion can induce cell vacuolization and cell death. Based on this feature, we performed a genome-wide CRISPR knockout screen in a cell-cell fusion model using Spike- and ACE2- expressing human cells to identify host factors that regulate syncytia formation. This approach correctly identified the known receptor ACE2. Additionally, we discovered other candidate genes. Experimental validation of these hits will be further conducted.

ALL ARE WELCOME

Should you have any enquiries, please feel free to contact Miss Cynthia Cheung at 3917 9748.