ArticlePLoS pathogens2022
A genetic screen identifies a protective type III interferon response to Cryptosporidium that requires TLR3 dependent recognition.
Article in PLoS pathogens, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 42 citations in OpenAlex.
- Microbiota-dependent interferon-λ controls immunity of the uterus and maternal-fetal interface.Research square · 2026Article
- Cas9-expressing HC-04 hepatocytes facilitate CRISPR-based analysis of Plasmodium falciparum sporozoite-host interactions.PLoS genetics · 2026Article
- Microbiota-dependent IFN-L controls uterine and placental immunity.bioRxiv : the preprint server for biology · 2026Article
- Mechanisms of Differential Signal Transduction by Interferon Lambda Receptor 1 Variants.Journal of innate immunity · 2026Article
- Pathogenicity and virulence ofVirulence · 2025Review
- Genetic crosses reveal genomic loci responsible for virulence in Cryptosporidium parvum infection.Cell reports · 2025Article
- Article
- Mechanisms of Differential Signal Transduction by IFNLR1 Variants.bioRxiv : the preprint server for biology · 2025Article
- Cryptosporidium parvum multidrug resistance protein confers resistance to toxic gut microbial metabolite.Cell host & microbe · 2025Article
- STAT1-IFITM3 promotes autophagy in epithelial cells to controlLife science alliance · 2025Article
- Article
- Evaluation of potential antiparasitic effect of ZnO nanoparticles on experimental cryptosporidiosis in immunosuppressed mice.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2025Article
- Expression and function of interferon lambda receptor 1 variants.FEBS letters · 2025Review
- Involvement of INS15 in the development and pathogenicity of the zoonotic pathogen Cryptosporidium parvum.PLoS neglected tropical diseases · 2024Article
- Host cell CRISPR genomics and modelling reveal shared metabolic vulnerabilities in the intracellular development of Plasmodium falciparum and related hemoparasites.Nature communications · 2024Article
- Analysis of intestinal epithelial cell responses to Cryptosporidium highlights the temporal effects of IFN-γ on parasite restriction.PLoS pathogens · 2024Article
- IFN-λ3 is induced byInfection and immunity · 2024Article
- Immunity to Cryptosporidium: insights into principles of enteric responses to infection.Nature reviews. Immunology · 2024Review
- Role of type-I and type-III interferons in gastrointestinal homeostasis and pathogenesis.Current opinion in immunology · 2024Review
- Human dendritic cell interactions with the zoonotic parasiteFrontiers in immunology · 2024Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Cryptosporidium is a leading cause of severe diarrhea and diarrheal-related death in children worldwide. As an obligate intracellular parasite, Cryptosporidium relies on intestinal epithelial cells to provide a niche for its growth and survival, but little is known about the contributions that the infected cell makes to this relationship. Here we conducted a genome wide CRISPR/Cas9 knockout screen to discover host genes that influence Cryptosporidium parvum infection and/or host cell survival. Gene enrichment analysis indicated that the host interferon response, glycosaminoglycan (GAG) and glycosylphosphatidylinositol (GPI) anchor biosynthesis are important determinants of susceptibility to C. parvum infection and impact on the viability of host cells in the context of parasite infection. Several of these pathways are linked to parasite attachment and invasion and C-type lectins on the surface of the parasite. Evaluation of transcript and protein induction of innate interferons revealed a pronounced type III interferon response to Cryptosporidium in human cells as well as in mice. Treatment of mice with IFNλ reduced infection burden and protected immunocompromised mice from severe outcomes including death, with effects that required STAT1 signaling in the enterocyte. Initiation of this type III interferon response was dependent on sustained intracellular growth and mediated by the pattern recognition receptor TLR3. We conclude that host cell intrinsic recognition of Cryptosporidium results in IFNλ production critical to early protection against this infection.
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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.