ArticleNature microbiology2023
Inflammatory monocytes promote granuloma control of Yersinia infection.
Article in Nature microbiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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.
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Who cites it
16 citing papers in PubMed, 18 citations in OpenAlex.
- Diverse infections transcriptionally reprogram the intestinal epithelium and epithelial-immune cell interactions.Nature immunology · 2026Article
- Article
- Alternatively activated monocyte-derived myeloid cells promote extracellular pathogen persistence in pulmonary fungal granulomas.The Journal of experimental medicine · 2026Article
- Hormonal rewiring of immunity during dietary restriction ensures host defense and systemic glucose conservation.Immunity · 2026Article
- In situ visualization of Clostridioides difficile phenotypic heterogeneity and single-cell morphology during gut infection.Nature communications · 2026Article
- Diverse infections transcriptionally reprogram the intestinal epithelium and epithelial-immune cell interactions.bioRxiv : the preprint server for biology · 2025Article
- Article
- Yersinia pseudotuberculosis growth arrest during type-III secretion system expression is associated with altered ribosomal protein expression and decreased gentamicin susceptibility.PLoS pathogens · 2025Article
- Current Challenges inMicroorganisms · 2025Review
- Loss of CXCR5 expression and monocyte epithelial-mesenchymal transition are blood-borne signatures of sterile granulomatous diseases.Clinical & translational immunology · 2025Article
- Polysaccharide hydrogels for skin wound healing.Heliyon · 2024Review
- Host stress drives tolerance and persistence: The bane of anti-microbial therapeutics.Cell host & microbe · 2024Review
- A TNF-IL-1 circuit controls Yersinia within intestinal pyogranulomas.The Journal of experimental medicine · 2024Article
- Article
- Article
- A TNF-IL-1 circuit controlsbioRxiv : the preprint server for biology · 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
12 authors at 2 institutions in 2 countries.
Funding
Abstract
Granulomas are organized immune cell aggregates formed in response to chronic infection or antigen persistence. The bacterial pathogen Yersinia pseudotuberculosis (Yp) blocks innate inflammatory signalling and immune defence, inducing neutrophil-rich pyogranulomas (PGs) within lymphoid tissues. Here we uncover that Yp also triggers PG formation within the murine intestinal mucosa. Mice lacking circulating monocytes fail to form defined PGs, have defects in neutrophil activation and succumb to Yp infection. Yersinia lacking virulence factors that target actin polymerization to block phagocytosis and reactive oxygen burst do not induce PGs, indicating that intestinal PGs form in response to Yp disruption of cytoskeletal dynamics. Notably, mutation of the virulence factor YopH restores PG formation and control of Yp in mice lacking circulating monocytes, demonstrating that monocytes override YopH-dependent blockade of innate immune defence. This work reveals an unappreciated site of Yersinia intestinal invasion and defines host and pathogen drivers of intestinal granuloma formation.
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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 Socratic graph.