ArticleCommunications biology2026
Ontogeny independent expression of LPCAT2 in granuloma macrophages during experimental visceral leishmaniasis.
Article in Communications biology, 2026. 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.
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Who cites it
1 citing paper in PubMed.
- Ontogeny independent expression of LPCAT2 in granuloma macrophages during experimental visceral leishmaniasis.Communications biology · 2026Article
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Authors and funding
13 authors.
Funding
Abstract
Granulomas are organized inflammatory lesions formed in response to persistent stimuli such as infections. Murine infection with Leishmania donovani results in granulomas in the liver, seeded by infected Kupffer cells, and serves as a well-defined model of infection-induced granuloma formation. The resolution of granulomatous inflammation requires dynamic shifts in immune-cell activation states, imposing metabolic demands. As mediators of cell signaling, lipid metabolism plays a key role in regulating inflammation and infection. How lipid changes are spatially linked to altered immune cell transcription remains unresolved. We performed a multimodal imaging analysis combining MALDI mass spectrometry, spatial and single cell transcriptomics, proteomics of flow-sorted macrophages and histopathology of L. donovani induced hepatic granulomas. Using this spatially-integrated approach, we identified LPCAT2-mediated membrane re-modelling of myeloid cells as a novel feature of these granulomas. Our study provides new insights into local immunometabolic changes associated with granuloma formation and macrophage activation.
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