Overview
- A Science paper published Monday shows that in mouse models Candida auris takes refuge in hair follicles and endures there far longer than Candida albicans by exposing chitin on its cell wall.
- The exposed chitin provokes a type 1 immune response with increased interferon-gamma (IFNγ) from cDC1, Tc1 and Th1 cells that signals to hair follicle keratinocytes and reduces IL-17–driven antifungal programs.
- IFNγ-driven signaling also slows normal hair follicle cell turnover, creating a niche of older, damaged cells where the fungus can persist and resist skin clearance.
- The mechanism helps explain why decolonization is difficult and why skin carriage fuels transmission in hospitals and nursing homes while public-health surveillance continues to record thousands of U.S. cases and high antifungal resistance.
- Researchers say early intervention ideas include drugs that shift immunity from IFNγ toward IL-17 or agents that block chitin, but these approaches are preclinical and require tests in human studies before changing infection-control practice.