The abstract is read at the publisher; the summary is JClub's.
HMB-PP–activated Vγ9Vδ2 human intestinal T-cells potently suppress Candida albicans growth in healthy organ cultures via an IL-22–dependent mechanism.
- Why it matters: Gut symbionts shape mucosal immunity, but the specific human microbes and pathways that restrain endogenous fungi—and how Crohn’s disease disrupts them—remain unclear.
- What they did: Human intestinal organ cultures were stimulated with bacterial metabolite HMB-PP to test Vδ2 T-cell control of C. albicans, using IL-22 dependence, ex vivo Crohn’s disease samples, and an intestine-on-a-chip invasion model.
- The result: In Crohn’s disease, Vδ2 T-cells poorly responded to HMB-PP, allowing filament-forming C. albicans to trigger neutrophil extracellular traps and macrophage IL-1β release, with CD-derived strains showing increased tissue adhesion and rapid barrier invasion.
The findingWhy it mattersWhat they didThe result
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