ArticlePLoS pathogens2013
Intestinal CD103+ dendritic cells are key players in the innate immune control of Cryptosporidium parvum infection in neonatal mice.
Article in PLoS pathogens, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 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
59 citing papers in PubMed, 101 citations in OpenAlex.
- Murine Intestinal Neonatal and Adult Dendritic Cell Subset Migration and Activation Characteristics in Response to Toll-Like Receptor Stimulation Through MyD88.Scandinavian journal of immunology · 2026Article
- Human immune response to primary cryptosporidiosis parallels murine infection models.Infection and immunity · 2026Article
- Early life infection withGut microbes · 2025Article
- Role of conventional dendritic cells in schistosomiasis-induced pulmonary hypertension.Clinical science (London, England : 1979) · 2025Article
- Administration of the NOD2 Agonist MDP Reduces Cryptosporidium parvum Infection in Neonatal Mice Through IL-22 Involvement.European journal of immunology · 2025Article
- Cryptosporidium parvum multidrug resistance protein confers resistance to toxic gut microbial metabolite.Cell host & microbe · 2025Article
- Deciphering Host-Pathogen Interactions: Role ofPathogens (Basel, Switzerland) · 2025Review
- Intestinal cDC1s provide cues required for CD4+ T cell-mediated resistance to Cryptosporidium.The Journal of experimental medicine · 2024Article
- Dendritic cell-mediated responses to secreted Cryptosporidium effectors promote parasite-specific CD8Mucosal immunology · 2024Article
- Immunity to Cryptosporidium: insights into principles of enteric responses to infection.Nature reviews. Immunology · 2024Review
- Medical prospects of cryptosporidiosisVeterinary world · 2024Article
- Characterization of intestinal mononuclear phagocyte subsets in young ruminants at homeostasis and duringFrontiers in immunology · 2024Article
- Article
- Intestinal cDC1s provide IL-12 dependent and independent functions required for CD4bioRxiv : the preprint server for biology · 2023Article
- Microbiota-produced indole metabolites disrupt mitochondrial function and inhibit Cryptosporidium parvum growth.Cell reports · 2023Article
- Microbiota produced indole metabolites disrupt host cell mitochondrial energy production and inhibitbioRxiv : the preprint server for biology · 2023Article
- Dendritic Cells andMicroorganisms · 2023Review
- Stromal regulation of the intestinal barrier.Mucosal immunology · 2023Review
- Cryptosporidium uses CSpV1 to activate host type I interferon and attenuate antiparasitic defenses.Nature communications · 2023Article
- Early immune and host cell responses toFrontiers in parasitology · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cryptosporidium parvum is a zoonotic protozoan parasite found worldwide, that develops only in the gastrointestinal epithelium and causes profuse diarrhea. Using a mouse model of C. parvum infection, we demonstrated by conditional depletion of CD11c+ cells that these cells are essential for the control of the infection both in neonates and adults. Neonates are highly susceptible to C. parvum but the infection is self-limited, whereas adults are resistant unless immunocompromised. We investigated the contribution of DC to the age-dependent susceptibility to infection. We found that neonates presented a marked deficit in intestinal CD103+ DC during the first weeks of life, before weaning, due to weak production of chemokines by neonatal intestinal epithelial cells (IEC). Increasing the number of intestinal CD103+ DC in neonates by administering FLT3-L significantly reduced susceptibility to the infection. During infections in neonates, the clearance of the parasite was preceded by a rapid recruitment of CD103+ DC mediated by CXCR3-binding chemokines produced by IEC in response to IFNγ. In addition to this key role in CD103+ DC recruitment, IFNγ is known to inhibit intracellular parasite development. We demonstrated that during neonatal infection CD103+ DC produce IL-12 and IFNγ in the lamina propria and the draining lymph nodes. Thus, CD103+DC are key players in the innate immune control of C. parvum infection in the intestinal epithelium. The relative paucity of CD103+ DC in the neonatal intestine contributes to the high susceptibility to intestinal infection.
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.