A groundbreaking study from the Hebrew University of Jerusalem has revealed that eosinophils, immune cells typically associated with allergies and asthma, also serve as key defenders against Candida albicans, a dangerous fungal pathogen. Published in Nature Communications, the research highlights a novel immune pathway that could pave the way for new treatments to bolster the body’s natural defenses against life-threatening fungal infections, a growing concern in healthcare settings worldwide.
Led by Professor Francesca Levi-Schaffer and conducted by PhD candidates Ilan Zaffran, Prince Ofori, and postdoctoral fellow Pratibha Gaur, the study uncovers how eosinophils recognize and combat Candida albicans, a fungus that poses severe risks to immunocompromised individuals. The research identifies the CD48 receptor on eosinophils as critical to this defense mechanism. CD48 binds to Als6, a fungal surface protein, enabling eosinophils to detect the pathogen and release proteins, such as major basic protein 1 (MBP-1), which inhibit fungal growth and survival.
Invasive Candida infections are notoriously difficult to treat, contributing to significant mortality in hospital settings. This discovery challenges the traditional view of eosinophils as primarily allergy-related cells, demonstrating their broader role in infection control. By identifying the CD48–Als6 pathway, the study opens new avenues for therapeutic strategies that could enhance natural immunity, offering hope for improved treatments for vulnerable patients.
The findings reshape our understanding of eosinophils’ role in the immune system and highlight their potential as allies in fighting fungal infections. With further research, this pathway could lead to innovative therapies that leverage the body’s own defenses to combat the rising threat of invasive Candida infections.
The research paper titled “Eosinophil 1 CD48 interactions with Candida albicans Als6 is protective in vitro and in mouse systemic candidiasis.” is now available in Nature Communications and can be accessed at https://www.nature.com/articles/s41467-025-64276-3
DOI 10.1038/s41467-025-64276-3 / MS NO. NCOMMS-23-29845
