ArticleJCI insight2017
Type I interferons regulate susceptibility to inflammation-induced preterm birth.
Article in JCI insight, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 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.
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
51 citing papers in PubMed, 70 citations in OpenAlex.
- Maternal gut microbiota mediates prenatal stress-induced fetal blood‒brain barrier dysfunction.Gut microbes · 2026Article
- Ambient temperature regulates CD4iScience · 2026Article
- Seizure phenotypes and short-term prognosis in neonatal lupus: a multicenter retrospective cohort in China.Frontiers in immunology · 2026Article
- Article
- The Chromosome 19 miRNA cluster guards trophoblasts against overacting innate immunity.Communications biology · 2025Article
- Persistent Human T-Lymphotropic Virus Type 1 (HTLV-1) Infection in the Placenta of Pregnant Women.Journal of medical virology · 2025Article
- Epigenetic profiling of preterm birth: a dual-tissue methylation patterns using long-read sequencing.Frontiers in epigenetics and epigenomics · 2025Article
- Lactobacillus crispatus S-layer proteins modulate innate immune response and inflammation in the lower female reproductive tract.Nature communications · 2024Article
- ADAR1 could be a potential diagnostic target for intrauterine infection patients.Scientific reports · 2024Article
- IL-1 and TNF mediates IL-6 signaling at the maternal-fetal interface during intrauterine inflammation.Frontiers in immunology · 2024Article
- Blockade of IL-6R prevents preterm birth and adverse neonatal outcomes.EBioMedicine · 2023Article
- Emerging role of toll-like receptors signaling and its regulators in preterm birth: a narrative review.Archives of gynecology and obstetrics · 2023Review
- Control of lupus activity during pregnancy via the engagement of IgG sialylation: novel crosstalk between IgG sialylation and pDC functions.Frontiers of medicine · 2023Article
- BAFF and APRIL counterregulate susceptibility to inflammation-induced preterm birth.Cell reports · 2023Article
- Pregnancy-associated systemic gene expression compared to a pre-pregnancy baseline, among healthy women with term pregnancies.Frontiers in immunology · 2023Article
- The Innate Defense in the Zika-Infected Placenta.Pathogens (Basel, Switzerland) · 2022Review
- Recent progress of interferon-tau research and potential direction beyond pregnancy recognition.The Journal of reproduction and development · 2022Review
- Mechanisms of immune regulation by the placenta: Role of type I interferon and interferon-stimulated genes signaling during pregnancy.Immunological reviews · 2022Review
- Interferon epsilon and preterm birth subtypes; a new piece of the type I interferon puzzle during pregnancy?American journal of reproductive immunology (New York, N.Y. : 1989) · 2022Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
23 authors at 6 institutions in 2 countries.
Funding
Abstract
Preterm birth (PTB) is a leading worldwide cause of morbidity and mortality in infants. Maternal inflammation induced by microbial infection is a critical predisposing factor for PTB. However, biological processes associated with competency of pathogens, including viruses, to induce PTB or sensitize for secondary bacterial infection-driven PTB are unknown. We show that pathogen/pathogen-associated molecular pattern-driven activation of type I IFN/IFN receptor (IFNAR) was sufficient to prime for systemic and uterine proinflammatory chemokine and cytokine production and induction of PTB. Similarly, treatment with recombinant type I IFNs recapitulated such effects by exacerbating proinflammatory cytokine production and reducing the dose of secondary inflammatory challenge required for induction of PTB. Inflammatory challenge-driven induction of PTB was eliminated by defects in type I IFN, TLR, or IL-6 responsiveness, whereas the sequence of type I IFN sensing by IFNAR on hematopoietic cells was essential for regulation of proinflammatory cytokine production. Importantly, we also show that type I IFN priming effects are conserved from mice to nonhuman primates and humans, and expression of both type I IFNs and proinflammatory cytokines is upregulated in human PTB. Thus, activation of the type I IFN/IFNAR axis in pregnancy primes for inflammation-driven PTB and provides an actionable biomarker and therapeutic target for mitigating PTB risk.
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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.