ArticleThe Journal of clinical investigation2015
CXCR3 blockade protects against Listeria monocytogenes infection-induced fetal wastage.
Article in The Journal of clinical investigation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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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.
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Who cites it
60 citing papers in PubMed, 86 citations in OpenAlex.
- Human labour is associated with altered regulatory T cell function and maternal immune activation.Clinical and experimental immunology · 2020Trial
- Maternal Krüppel-like factor 2 (KLF2)+ CD4 T cells promote fertility and fetal tolerance.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
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- Innate immune responses to pathogens at the maternal-fetal interface.Nature reviews. Immunology · 2025Review
- Neutrophils at the Maternal-Fetal Interface: Agents of Protection or Destruction?American journal of reproductive immunology (New York, N.Y. : 1989) · 2025Review
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- Vaginal host immune-microbiome-metabolite interactions associated with spontaneous preterm birth in a predominantly white cohort.NPJ biofilms and microbiomes · 2025Article
- Maternal microchimeric cell trafficking and its biological consequences depend on the onset of inflammation at the feto-maternal interface.Seminars in immunopathology · 2025Review
- Immune suppression sustained allograft acceptance requires PD1 inhibition of CD8+ T cells.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- CD4+ but not CD8+ T cells are required for protection against severe guinea pig cytomegalovirus infections.PLoS pathogens · 2024Article
- Article
- Impact of SARS-CoV-2 infection during pregnancy on the placenta and fetus.Seminars in perinatology · 2024Review
- Aberrant CD8Frontiers in immunology · 2024Article
- Beyond Immune Balance: The Pivotal Role of Decidual Regulatory T Cells in Unexplained Recurrent Spontaneous Abortion.Journal of inflammation research · 2024Review
- Crossing the Barrier: A Comparative Study ofCells · 2023Review
- Reproductive outcomes after pregnancy-induced displacement of preexisting microchimeric cells.Science (New York, N.Y.) · 2023Article
- Alternate-Day Fasting Ameliorates Newly Established Sjögren's Syndrome-like Sialadenitis in Non-Obese Diabetic Mice.International journal of molecular sciences · 2022Article
- Genetics, epigenetics, and transcriptomics of preterm birth.American journal of reproductive immunology (New York, N.Y. : 1989) · 2022Review
- Article
- Trophoblast antigens, fetal blood cell antigens, and the paradox of fetomaternal tolerance.The Journal of experimental medicine · 2022Article
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8 authors at 1 institution in 2 countries.
Funding
Abstract
Mammalian pregnancy requires protection against immunological rejection of the developing fetus bearing discordant paternal antigens. Immune evasion in this developmental context entails silenced expression of chemoattractant proteins (chemokines), thereby preventing harmful immune cells from penetrating the maternal-fetal interface. Here, we demonstrate that fetal wastage triggered by prenatal Listeria monocytogenes infection is driven by placental recruitment of CXCL9-producing inflammatory neutrophils and macrophages that promote infiltration of fetal-specific T cells into the decidua. Maternal CD8+ T cells with fetal specificity upregulated expression of the chemokine receptor CXCR3 and, together with neutrophils and macrophages, were essential for L. monocytogenes-induced fetal resorption. Conversely, decidual accumulation of maternal T cells with fetal specificity and fetal wastage were extinguished by CXCR3 blockade or in CXCR3-deficient mice. Remarkably, protection against fetal wastage and in utero L. monocytogenes invasion was maintained even when CXCR3 neutralization was initiated after infection, and this protective effect extended to fetal resorption triggered by partial ablation of immune-suppressive maternal Tregs, which expand during pregnancy to sustain fetal tolerance. Together, our results indicate that functionally overriding chemokine silencing at the maternal-fetal interface promotes the pathogenesis of prenatal infection and suggest that therapeutically reinforcing this pathway represents a universal approach for mitigating immune-mediated pregnancy complications.
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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 Socratic graph.