Research team

Expertise

My research expertise lies at the intersection of innate immunity, epithelial cell biology, and host-pathogen interactions, with a particular focus on inflammasome signaling pathways. My work centers on understanding how barrier epithelial cells—particularly keratinocytes—sense and respond to pathogenic threats through inflammasome activation. During my PhD, I investigated the distinct regulatory mechanisms of two key inflammasome sensors, human NLRP1 and NLRP3, in skin epithelial cells.This work highlighted the tissue-specific control of inflammasome pathways and how barrier cells balance immune vigilance with tolerance to daily environmental exposure. Prior to my PhD, I worked as a research assistant on bat immunology, exploring how bats—natural viral reservoirs—tolerate high viral loads without overt inflammation. I was involved in characterizing the NLRP3 inflammasome in bat immune cells and used both in vitro and in vivo approaches, including a “bat-tized” mouse model, to assess viral pathogenesis and immune regulation. My current research interests continue to evolve around inflammasome biology, epithelial immunology, and host-pathogen interactions, with a growing focus on applying this knowledge to understand tissue-specific immunity and develop targeted immunotherapies.

The Epithelial NLRP3 Inflammasome: A New Frontier in Innate Immunity (EpiSome). 01/10/2026 - 30/09/2027

Abstract

The NLRP3 inflammasome is a multi-protein complex and a central component of the innate immune system, functioning as a sentinel that detects a broad spectrum of threats within a host cell. While vital for host defense against pathogens, excessive NLRP3 inflammasome activity is a key driver for various autoinflammatory and chronic inflammatory diseases. Therefore, its activation is a tightly regulated, two-step process that requires a priming signal to prepare the cell and a subsequent activation signal to trigger its inflammatory actions. Once activated, the inflammasome processes pro-inflammatory cytokines into their active forms and induces an inflammatory form of cell death known as pyroptosis, making it a critical target for therapeutic intervention. Despite this, research on the NLRP3 inflammasome has focused almost exclusively on its function in immune cells, leaving a critical knowledge gap regarding its role in epithelial cells. This proposal seeks to bridge that gap by investigating a novel activation pathway discovered in human epithelial cells. The objective of this research is to elucidate the molecular mechanisms underlying the unique priming as well as activation pathway that governs epithelial NLRP3 inflammasome activity. Ultimately, this study will provide a crucial foundation for developing novel therapies for inflammatory diseases that originate at epithelial barriers.

Researcher(s)

Research team(s)

Funding

  • BOF

Project type(s)

  • Research Project