ArticleImmunology2015
Interleukin-22 and CD160 play additive roles in the host mucosal response to Clostridium difficile infection in mice.
Article in Immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
22 citing papers in PubMed, 23 citations in OpenAlex.
- Balancing act of cytokines in controlling the severity ofInfection and immunity · 2026Review
- High-fat diet rewires gut host-microbiota relationship to derive worse outcomes followingbioRxiv : the preprint server for biology · 2026Article
- Therapeutic activation of IL-22-producing innate lymphoid cells enhances host defenses to Clostridioides difficile infection.Cell reports · 2025Article
- Polyamines and hypusination are important forInfection and immunity · 2023Article
- Epithelial HVEM maintains intraepithelial T cell survival and contributes to host protection.Science immunology · 2022Article
- Microbiota-mediated protection against antibiotic-resistant pathogens.Genes and immunity · 2021Review
- Article
- The role of innate lymphoid cells in response to microbes at mucosal surfaces.Mucosal immunology · 2020Review
- Interleukin-22-mediated host glycosylation prevents Clostridioides difficile infection by modulating the metabolic activity of the gut microbiota.Nature medicine · 2020Article
- Acetate coordinates neutrophil and ILC3 responses against C. difficile through FFAR2.The Journal of experimental medicine · 2020Article
- Type 3 Immunity during Clostridioides difficile Infection: Too Much of a Good Thing?Infection and immunity · 2019Review
- Article
- CD160 Stimulates CD8ImmunoHorizons · 2018Article
- LIGHT-HVEM Signaling in Innate Lymphoid Cell Subsets Protects Against Enteric Bacterial Infection.Cell host & microbe · 2018Article
- Systemic Inflammatory Responses in Ulcerative Colitis Patients and Clostridium difficile Infection.Digestive diseases and sciences · 2018Observational
- Role of the leukocyte response in normal and immunocompromised host after Clostridium difficile infection.Anaerobe · 2017Review
- Role of interferon-γ and inflammatory monocytes in driving colonic inflammation during acute Clostridium difficile infection in mice.Immunology · 2017Article
- Clostridium difficile colitis: pathogenesis and host defence.Nature reviews. Microbiology · 2016Review
- Neutrophil-mediated inflammation in the pathogenesis of Clostridium difficile infections.Anaerobe · 2016Review
- Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Our previous work has shown the significant up-regulation of Il22 and increased phosphorylation of signal transducer and activator of transcription 3 (STAT3) as part of the mucosal inflammatory response to Clostridium difficile infection in mice. Others have shown that phosphorylation of STAT3 at mucosal surfaces includes interleukin-22 (IL-22) and CD160-mediated components. The current study sought to determine the potential role(s) of IL-22 and/or CD160 in the mucosal response to C. difficile infection. Clostridium difficile-infected mice treated with anti-IL-22, anti-CD160 or a combination of the two showed significantly reduced STAT3 phosphorylation in comparison to C. difficile-infected mice that had not received either antibody. In addition, C. difficile-infected mice treated with anti-IL-22/CD160 induced a smaller set of genes, and at significantly lower levels than the untreated C. difficile-infected mice. The affected genes included pro-inflammatory chemokines and cytokines, and anti-microbial peptides. Furthermore, histopathological and flow cytometric assessments both showed a significantly reduced influx of neutrophils in C. difficile-infected mice treated with anti-IL-22/CD160. These data demonstrate that IL-22 and CD160 are together responsible for a significant fraction of the colonic STAT3 phosphorylation in C. difficile infection. They also underscore the additive effects of IL-22 and CD160 in mediating both the pro-inflammatory and pro-survival aspects of the host mucosal response in this infection.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.