Overview of eosinophil extracellular trap cell death and recent advances in research

Abstract

Eosinophil extracellular trap cell death (EETosis) is characterized by the release of nuclear or mitochondrial DNA by eosinophils, forming complex structures with granular proteins to capture pathogens and modulate tissue damage. Recent findings have highlighted EETosis as a key mechanism in various pathological conditions, such as in excessive mucus formation and tissue injury in eosinophilic chronic rhinosinusitis, and its antitumor effects in diseases such as colorectal cancer. Additionally, the involvement of eosinophil-specific proteins, such as galectin-10 and Charcot-Leyden crystals, has garnered attention along with the development of cfDNA scavengers and the advent of single-cell RNA sequencing techniques, both of which are driving advances in understanding the molecular basis of EETosis and its regulatory pathways. This review provides an overview of the historical context, molecular mechanisms, and pathological significance of EETosis in diverse immune and inflammatory responses, including tumor immunity. Furthermore, the potential for novel therapeutic strategies targeting EETosis is discussed, shedding light on future directions for managing chronic inflammatory diseases and malignancies.