Highlights of IMMUNOLOGY2026™ - Invited Program Recordings-At the crossroads of IL-17 signaling_ IL-17 signal transduction in autoimmunity and fungal infections

At the crossroads of IL-17 signaling_ IL-17 signal transduction in autoimmunity and fungal infections

Video Transcription

Video Summary

The speaker, a signaling researcher turned fungal immunologist, summarized nearly two decades of work on IL-17 and related cytokines in antifungal immunity, especially against <em>Candida albicans</em>. In the oral cavity, they showed that IL-17 acts mainly on superficial keratin-13 epithelial cells, while IL-22 acts on deeper keratin-14 stem-like cells to promote tissue repair and replenishment. Both cytokines are needed for full protection, and downstream signaling involves ACT1 and IκBζ, which drive antimicrobial peptides like defensins and chemokines that recruit neutrophils.

The talk also described new single-cell RNA-seq work revealing dynamic epithelial changes during oral candidiasis, including shifts from basal to suprabasal cell states as infection resolves.

In contrast, vaginal candidiasis was presented as a more complex case. Despite earlier evidence suggesting IL-17 was dispensable, the lab found that combined loss of IL-17 and IL-22 signaling makes mice highly susceptible to vulvovaginal candidiasis, regardless of estrogen status. This points to a cooperative, immune-driven protective pathway that can be separate from hormone-driven disease susceptibility.

The speaker concluded that tissue-specific IL-17/IL-22 responses shape antifungal defense differently across mucosal sites, and that there is still much to learn about the transcriptional programs and cell types involved.

Keywords

IL-17

IL-22

antifungal immunity

Candida albicans

oral candidiasis

vulvovaginal candidiasis

single-cell RNA-seq