ArticleMucosal immunology2022
Enterocyte-innate lymphoid cell crosstalk drives early IFN-γ-mediated control of Cryptosporidium.
Article in Mucosal immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
41 citing papers in PubMed.
- Diverse infections transcriptionally reprogram the intestinal epithelium and epithelial-immune cell interactions.Nature immunology · 2026Article
- Intestinal Epithelial MHC-II at the Interface of Microbiota, Immunity, and Inflammation.International journal of molecular sciences · 2026Review
- Human immune response to primary cryptosporidiosis parallels murine infection models.Infection and immunity · 2026Article
- Mouse Models for Use in Cryptosporidium Infection Studies, Quantification of Parasite Burden Using Flow Cytometry, qPCR and Histopathology, and Confocal Imaging of Oocysts.Methods in molecular biology (Clifton, N.J.) · 2026Article
- Early life infection withGut microbes · 2025Article
- Pathogenicity and virulence ofVirulence · 2025Review
- Article
- Long non-coding RNA U90926 modulates IFN-γ-stimulated gene transcription and cell-intrinsic anti-Infection and immunity · 2025Article
- Administration of the NOD2 Agonist MDP Reduces Cryptosporidium parvum Infection in Neonatal Mice Through IL-22 Involvement.European journal of immunology · 2025Article
- Decrease in Incidence of Diarrhea Due to Cryptosporidium in Bangladeshi Children Is Associated With an Increase in Anti-Cryptosporidium Antibody Avidity.The Journal of infectious diseases · 2025Observational
- STAT1-IFITM3 promotes autophagy in epithelial cells to controlLife science alliance · 2025Article
- Environmental stress drives clearance of a persistent enteric virus in mice.Nature microbiology · 2025Article
- De-coupling immune parameters and toxicity associated with IL-12 agonism.Cell reports · 2025Article
- Article
- Article
- Intestinal cDC1s provide cues required for CD4+ T cell-mediated resistance to Cryptosporidium.The Journal of experimental medicine · 2024Article
- Intraepithelial Lymphocytes of the Intestine.Annual review of immunology · 2024Review
- Dendritic cell-mediated responses to secreted Cryptosporidium effectors promote parasite-specific CD8Mucosal immunology · 2024Article
- Analysis of intestinal epithelial cell responses to Cryptosporidium highlights the temporal effects of IFN-γ on parasite restriction.PLoS pathogens · 2024Article
- Immunity to Cryptosporidium: insights into principles of enteric responses to infection.Nature reviews. Immunology · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
Abstract
The intestinal parasite, Cryptosporidium, is a major contributor to global child mortality and causes opportunistic infection in immune deficient individuals. Innate resistance to Cryptosporidium, which specifically invades enterocytes, is dependent on the production of IFN-γ, yet whether enterocytes contribute to parasite control is poorly understood. In this study, utilizing a mouse-adapted strain of C. parvum, we show that epithelial-derived IL-18 synergized with IL-12 to stimulate innate lymphoid cell (ILC) production of IFN-γ required for early parasite control. The loss of IFN-γ-mediated STAT1 signaling in enterocytes, but not dendritic cells or macrophages, antagonized early parasite control. Transcriptional profiling of enterocytes from infected mice identified an IFN-γ signature and enrichment of the anti-microbial effectors IDO, GBP, and IRG. Deletion experiments identified a role for Irgm1/m3 in parasite control. Thus, enterocytes promote ILC production of IFN-γ that acts on enterocytes to restrict the growth of Cryptosporidium.
Indexed as
Identifiers
What OpenQuestion holds
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.