My name is Pengjun Xi and I am a final-year PhD student at Karolinska Institute in Sweden. I am writing to apply for the Hong Kong Laureate Forum 2025.

My strong interest in attending the forum comes from my enthusiasm of science and the potential opportunities to talk to other young scientists worldwide as well as the collaboration opportunities with them. My current PhD project is working on innate-adaptive immune synergy in malaria. More specifically, the project aims to understand how antibodies, derived from the adaptive immune system, potentiate and control innate responses, focusing on natural killer (NK) cells, to malaria parasites in human patients. To do this I use single-cell RNA sequencing to identify changes in the transcriptome of different immune cell subsets over time after acute malaria. I then connect these changes to function by using advanced single-cell culture assays with live cell imaging, and flow cytometry of stimulated and co-cultured cells, as well as running Luminex to assess the parasite-specific antibody dynamics

I hope to be considered for this forum, where I could meet young generation scientists, exchange ideas, explore the potentials of collaboration. I also wish to appreciate the beauty of Hong Kong.

Karolinska Institute

Introduction: Natural killer (NK) cells are crucial in bridging innate and adaptive immunity during malaria infection. While different NK subsets have distinct roles and may exhibit memory upon reinfection, their regulation post-infection remains unclear. This study uses longitudinal samples from malaria-infected individuals to examine how infection affects NK cell diversity and function over time.

Methods: The cohort includes individuals with primary and prior malaria exposure. Blood samples were collected at diagnosis and at 10 days, 1, 3, 6, and 12 months post-diagnosis. PBMCs were analyzed for NK cell phenotypes via flow cytometry and targeted single-cell RNA sequencing. NK cytotoxicity was assessed using live cell imaging and flow cytometry.

Results: A marked reduction in total CD56+ NK cells was observed during acute infection, regardless of prior exposure. NK cells from this phase showed enhanced killing ability and upregulated expression of cytotoxic effectors PRF1 and GZMB. Elevated plasma granzyme B further supported increased cytotoxic function during acute malaria.

Conclusion: Acute malaria transiently boosts NK cell cytotoxicity, suggesting a key role in early immune response. Identifying signals driving this activation may aid malaria control strategies.