ArticleInfection and immunity2005
Th1 cytokines are essential for placental immunity to Listeria monocytogenes.
Article in Infection and immunity, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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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
20 citing papers in PubMed, 37 citations in OpenAlex.
- Fetal and neonatal demise in zoonotic diseases: pathology and pathogenesis.Infection and immunity · 2026Review
- VNUT-mediated ATP release suppresses T helper 1 (TScience advances · 2025Article
- Listeriosis.Nature reviews. Disease primers · 2025Review
- Histologic and molecular features shared between antibody-mediated rejection of kidney allografts and chronic histiocytic intervillositis support common pathogenesis.The Journal of pathology · 2025Article
- Article
- Kinetics of Placental Infection by Different SmoothPathogens (Basel, Switzerland) · 2022Article
- Plausibility of trophoblastic-like regulation of cancer tissue.Cancer management and research · 2019Article
- Adjuvant Potential of Poly-α-l-Glutamine from the Cell Wall of Mycobacterium tuberculosis.Infection and immunity · 2018Article
- Vertical Transmission ofPathogens (Basel, Switzerland) · 2018Review
- Placenta-on-a-chip: a novel platform to study the biology of the human placenta.The journal of maternal-fetal & neonatal medicine : the official journal of the European Association of Perinatal Medicine, the Federation of Asia and Oceania Perinatal Societies, the International Society of Perinatal Obstetricians · 2016Article
- Perinatal Listeria monocytogenes susceptibility despite preconceptual priming and maintenance of pathogen-specific CD8(+) T cells during pregnancy.Cellular & molecular immunology · 2014Article
- Regulatory T cells and the immune pathogenesis of prenatal infection.Reproduction (Cambridge, England) · 2013Review
- Reactive oxygen species-triggered trophoblast apoptosis is initiated by endoplasmic reticulum stress via activation of caspase-12, CHOP, and the JNK pathway in Toxoplasma gondii infection in mice.Infection and immunity · 2012Article
- Listeria monocytogenes cytoplasmic entry induces fetal wastage by disrupting maternal Foxp3+ regulatory T cell-sustained fetal tolerance.PLoS pathogens · 2012Article
- Up regulation of the maternal immune response in the placenta of cattle naturally infected with Neospora caninum.PloS one · 2011Article
- The Key Events Dose-Response Framework: its potential for application to foodborne pathogenic microorganisms.Critical reviews in food science and nutrition · 2009Article
- Colony-stimulating factor-1-dependent macrophage functions regulate the maternal decidua immune responses against Listeria monocytogenes infections during early gestation in mice.Infection and immunity · 2009Article
- Listeria-based HPV-16 E7 vaccines limit autochthonous tumor growth in a transgenic mouse model for HPV-16 transformed tumors.Vaccine · 2008Article
- Upregulation of cytokines is detected in the placentas of cattle infected with Neospora caninum and is more marked early in gestation when fetal death is observed.Infection and immunity · 2008Article
- Maternal vaccination: moving the science forward.Human reproduction updateReview
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The fetal allograft poses an immunological challenge: how is it protected while immunity to pathogens, particularly those that replicate in the placenta, is maintained? Several theories have been proposed to explain this fetal protection, including a pregnancy-based bias towards a Th2 rather than Th1 cytokine profile in order to avoid generating cytotoxic T cells that could threaten the fetus. Listeria monocytogenes preferentially replicates in the placenta and systemically requires a Th1 response for sterile eradication. In the placenta, the Th1 cytokines tumor necrosis factor alpha (TNF-alpha) and gamma interferon (IFN-gamma) are also synthesized in response to this pathogen, without fetal loss. Here we show, by using mice homozygous for null mutations in either the cytokine or cytokine receptor genes, a requirement for both TNF-alpha and IFN-gamma signaling for an effective placental immune response to L. monocytogenes. However, T cells were not recruited to the placenta. Genetic studies in which the fetal component of the placenta was genetically different from the mother indicated that both the production of and response to these cytokines were maternal. Despite the requirement for these cytokines, the early recruitment of neutrophils to the placenta was normal. Consequently, the bacterium appeared to be delayed in its colonization of this organ and did not fully gain hold until 72 h postinfection. These data show a requirement for Th1 cytokines during pregnancy for effective immunity and indicate that a bias away from Th1 cytokine synthesis is not a necessary prerequisite of pregnancy.
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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.