I am currently an NHMRC Emerging Leadership Fellow and Head of the Post-Cell Death Biology and Immunology Laboratory, leading an internationally recognised research program investigating post-cell death biology and its roles in inflammatory diseases. I have established research independence through 45 publications (including 20 first and senior-author papers) in leading international journals, >7,000 citations, and >$1.5M in competitive funding as CIA. I lead a multidisciplinary research team, supervising 1 RA, 11 PhD, 3 Masters and 3 Honours students to date. My growing reputation is reflected by invited presentations at major international conferences, co-chairing the Gordon Research Seminar on Cell Death, NHMRC grant review, editorial responsibilities, ASMR State Convenor and multidisciplinary collaborations.

My research program has generated sustained knowledge impact by redefining cell death as an active regulator of innate immunity, inflammation and disease, through 3 interconnected arms spanning innate immune-mediated cell death, post-cell death biology, and their translation to infection and autoimmunity. These discoveries have generated ~7,000 citations (FWCI 14.04), demonstrating broad multidisciplinary influence.

DEFINING LIPID-MEDIATED INNATE IMMUNE CELL DEATH

Host defence peptides constitute a major component of innate immunity and provide the first line of defence against pathogens and tumour cells. My research (including Sci Adv, Nat Comm x2, Oncotarget, Immunol Cell Biol) established lipid targeting as a conserved mechanism by which innate immune effectors execute cell death, thus advancing understanding of how these peptides eliminate pathogens and tumor cells. This work established the molecular basis of lipid-mediated fungal and tumour cell death, providing the first atomic insights into phospholipid-targeted membrane disruption. These findings were featured in field-positioning reviews, such Small, Signal Transduct. Target. Ther. It inspired >30 subsequently reported lipid-peptide interactions, underpinned three patents, and was adopted for preclinical therapeutic testing. Its reach and impact are further reflected by invited reviews e.g., Trends Pharmacol Sci, Cell Death Differ, an invited editor for Special Issue in Frontiers Immunol ((29 articles, 183 authors, ~300,000 views, >91,000 downloads), media reports, outreach and awarded presentations.

PIONEERING POST-CELL DEATH BIOLOGY

My research established post-cell death biology as a regulated process through which dying cells communicate with the immune system. A major pathway to impact was development of a flow cytometry methodology for detecting and isolating apoptotic cell-derived large extracellular vesicles (called “apoptotic bodies”), subsequently commercialised by Cayman Chemical and adopted by other investigators, including in a Cell study. Building upon this platform, my research established the conceptual and mechanistic framework of post-cell death biology by establishing defining features of apoptotic bodies (J Extracell Vesicles), identifying key regulators of apoptotic body formation (Cell Reports, Front Immunol), uncovering mechanisms controlling apoptotic body cargo packaging and membrane integrity (J Proteomics; Cell Death Dis; Front Immunol) and linking apoptotic body formation to regulation of efferocytosis (i.e. dead cell clearance) (Cell Death Differ). The reach of this research is reflected by incorporation into the International Society for Extracellular Vesicles (ISEV) position statement and guidelines [29], an invited review in Trends Cell Biol. defining apoptotic extracellular vesicle, and exceptional influence within the rapidly growing extracellular vesicle field (SciVal Topic FWCI 42.46, prominence percentile 99.96).

TRANSLATING POST-CELL DEATH BIOLOGY TO INFECTION AND AUTOIMMUNITY

The mechanistic framework established above has enabled translation of post-cell death biology into clinically relevant infection and autoimmune diseases. This work demonstrated that efferocytosis of apoptotic bodies and defective cell clearance actively regulate host-pathogen interactions and autoimmune responses, thus linking post-cell death biology to disease. My findings first demonstrated that apoptotic bodies mediate bystander influenza A virus propagation (Commun Biol). Furthermore, I identified efferocytosis of infected cell corpses as a novel ACE2-independent pathway for SARS-CoV-2 infection and inflammation (Nat Commun), leading to identification of apoptotic body formation inhibitors as candidate host-directed therapeutics for COVID-19. The concept has since been independently extended to African swine fever virus (PNAS), demonstrating its broader relevance across viral infections. Moreover, my recent findings also linked defective efferocytosis of apoptotic bodies to macrophage activation, atypical memory B cell expansion and autoimmune responses thus providing new insights into Sjögren's disease pathogenesis (bioRxiv). The translational impact of this program is reflected by Altmetric scores up to the 99th percentile, widespread coverage by international science media (including Science Daily, Phys.org, Technology Networks, The Conversation and IBTimes Singapore), and invited presentations spanning basic science and clinical communities, including the ASI2024, KAI2025 (Outstanding Presentation Award), Gordon Research Conference on Cell Death 2026 and leading immunology and rheumatology meetings.