ArticleCell reports2025
Therapeutic activation of IL-22-producing innate lymphoid cells enhances host defenses to Clostridioides difficile infection.
Article in Cell reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
9 citing papers in PubMed.
- The gut microbiota as a regulator of intestinal stem-cell fate: bacterial and fungal control of differentiation and regeneration.Gut microbes · 2026Review
- Building and regenerating intestines by manipulating intestinal stem cells.Nature reviews. Gastroenterology & hepatology · 2026Review
- Early-life colonization withScience (New York, N.Y.) · 2026Article
- Balancing act of cytokines in controlling the severity ofInfection and immunity · 2026Review
- Current Status of Intestinal Stem Cell Research: Mechanisms, Intestinal Diseases, and Organoid Development.Cells · 2026Review
- Intestinal stem cells as innate immune sentinels: coupling environmental sensing to epithelial adaptation.Frontiers in immunology · 2026Review
- Gut microbiota in Henoch-Schönlein purpura: from pathogenesis to therapeutic strategies.Frontiers in immunology · 2026Review
- Review
- Intestinal IL-22RA1 signaling regulatesFrontiers in microbiology · 2025Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Clostridioides difficile causes debilitating colitis via secreted toxins that disrupt the intestinal barrier, and toxemia is associated with severe disease. Thus, therapies that fortify the intestinal barrier will reduce the severity of infection. Innate lymphoid cells (ILCs) are critical in the defense against acute C. difficile infection and represent a promising therapeutic target to limit disease. Here, we report that oral administration of the Toll-like receptor (TLR) 7 agonist R848 limits intestinal damage and protects mice from lethal C. difficile infection without impacting pathogen burden or altering the intestinal microbiome. R848 induced interleukin (IL)-22 secretion by ILCs, leading to STAT3 phosphorylation in the intestinal epithelium and increased stem cell proliferation. Genetic ablation of ILCs, IL-22, or epithelial-specific STAT3 abrogated R848-mediated protection. R848 reduced intestinal permeability following infection and limited systemic toxin dissemination. Combined, these data identify an immunostimulatory molecule that activates IL-22 production in ILCs to enhance host tissue defenses following C. difficile infection.
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Registered trials
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