Assistant Professor Chen Kaiwen

Research Interest

Myeloid cells such as macrophages and neutrophils express a repertoire of pattern recognition receptors to protect against microbial invasion, however, dysregulation in these pathways are increasingly recognised to drive autoinflammatory diseases.
Our laboratory studies the mechanisms by which inflammation is initiated and terminated by the innate immune system. A major interest of the lab is to understand how various programmed cell death pathways including apoptosis, pyroptosis and necroptosis are initiated during microbial infection and consequently how these death pathways promote host immunity in vivo. We also use a range of microbial mutants to define the corresponding microbial subversion mechanisms. The knowledge gained from these studies will improve our understanding of host-pathogen interactions and may unravel novel antimicrobial therapeutics and regulations of inflammation.

Recent Publications

1. Chan FHM, Yeap HW, Liu Z, Rosli SN, Low KE, Bonne I, Wu Y, Chong SZ and Chen KW. Plasticity of cell death pathways ensures GSDMD activation during Yersinia pseudotuberculosis infection. Cell Reports, 2025, in press.
2. Chen KW and Broz P. Gasdermins as evolutionarily conserved executors of inflammation and cell death. Nat Cell Bio, 2024, 26, 394–1406.
3. Yow SJ, Rosli SN, Hutchinson PE, Chen KW. Differential signalling requirements for RIPK1-dependent pyroptosis in neutrophils and macrophages. Cell Death Dis, 2024, 15:479
4. Chen KW, Demarco B, Ramos S, Heilig R, Goris M, Grayczyk JP, Assenmacher CA, Radaelli E, Joannas LD, Henao-Mejia J, Tacchini-Cottier F, Brodsky IE, Broz P. RIPK1 activates distinct gasdermins in macrophages and neutrophils upon pathogen blockade of innate immune signalling. PNAS, 2021, 118(28).
5. Demarco B, Grayczyk JP, Bjanes E, Le Roy D, Tonnus W, Assenmacher C-A, Radaelli E, Fettrelet T, Mack V, Linkermann A, Roger T, Brodsky IE, Chen KW, Broz P. Caspase-8-dependent gasdermin D cleavage promotes anti-microbial defence but confers susceptibility to TNF-induced lethality. Sci Adv, 2020, 6.