Pathogen–host interactions and safeguard mechanisms are important for combating external insults to the organism, but fungal interactions remain largely unknown. Drosophila melanogaster has been an important model for better understanding fungal immunity, but the knowledge of how parasites circumvent host defenses is limited. A study in Cell Reports now sheds light on how fungal pathogens can suppress host immunity in Drosophila by targeting β-glucan recognition proteins, which are part of the recognition system for fungal infection. When researchers assessed mutant response to fungal infection, they showed that GL3, a protein that had a previously unknown function, was essential for antifungal immunity, as GL3 mutants died much faster than other mutants. These new insights contribute to a better understanding of Drosophila antifungal immunity and the host–pathogen relationship. With immunity pathways having some degree of conservation between species, these results can open doors to identifying anti-fungal therapies.
Original reference: Lu, M. et al. Cell Rep. 43, 113642 (2024)
This is a preview of subscription content, access via your institution