Myo1f, an unconventional long-tailed class Ⅰ myosin, is crucial in multiple biological processes. It is involved in immune cell motility, innate antifungal immunity, and the regulation of immune-related signaling pathways. It plays a role in the adhesion and migration of various immune cells, and is associated with pathways like microtubule acetylation, mast cell degranulation, and T-cell activation and metabolism [1-3, 5-9].

Myo1f-deficient mice are more susceptible to systemic Candida albicans infections, indicating its importance in antifungal immunity. The absence of Myo1f in mice affects γδT intraepithelial lymphocyte homing, adhesion, and migration due to reduced CCR9 and α4β7 surface expression. T-cell-specific Myo1f knockout mice exhibit an increased tumor burden and attenuated EAE severity due to impaired T-cell activation. In Aspergillus fumigatus keratitis mouse models, knockdown of Myo1f reduces disease severity, decreases neutrophil and macrophage recruitment, and suppresses the MyD88/NF-κB signaling pathway [1,2,3,4].

In conclusion, Myo1f is essential for immune cell functions such as adhesion, migration, and activation, and is involved in antifungal immunity and the regulation of T-cell metabolism. Studies using Myo1f knockout or knockdown mouse models have revealed its role in fungal infections, tumor-related immune responses, and inflammatory diseases, providing insights into potential therapeutic targets for these conditions.