ArticleJournal of leukocyte biology2025
Differential roles for Irgm1 in myeloid cells for immune resistance to pathogenic bacteria.
Article in Journal of leukocyte biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Neutrophil Irgm1 ameliorates sepsis-induced myocardial dysfunction by promoting Alox15 degradation.Redox biology · 2026Article
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Authors and funding
10 authors.
Funding
Abstract
IRGM proteins are associated with increased susceptibility to Crohn's disease, mycobacterial infections, sepsis, and other inflammatory diseases, but the cells in which they function in vivo have not been delineated. To address this, mice with conditional deletions of Irgm1 were created and challenged with model pathogens. Irgm1fl/flLyz2-Cre+ mice (a myeloid deletion) displayed marked susceptibility to infections with Salmonella typhimurium, Listeria monocytogenes, and Toxoplasma gondii, paralleling those of global Irgm1-/- mice. However, infections of Irgm1fl/flLyz2-Cre+ mice with Citrobacter rodentium showed no increase in susceptibility, contrasting with marked increases in Irgm1fl/flVav-Cre+ mice (a hematopoietic deletion). Macrophages from Irgm1fl/flLyz2-Cre+ mice displayed pathologies present in macrophages from global Irgm1-/- mice, validating the conditional deletion in myeloid cells. These results suggest that Irgm1 functioning in myeloid cells is critical for immune resistance to intracellular pathogens, while Irgm1 functioning in additional hematopoietic population(s) is required for resistance to extracellular pathogens in the intestinal lumen.
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Registered trials
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