ArticleiScience2025
Malaria-derived hemozoin skews dendritic cell responses to bacterial infections by reducing interferon gene-transcription by SWI/SNF-NuRD.
Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed.
- Membrane-Targeted Consequences of Acetaminophen Toxicity and Off-Target Effects of Antimicrobial Peptides on Host Cell Membranes.International journal of molecular sciences · 2026Review
- Article
- Role of PBAF and Mediator kinase module in the RELA-dependent activation ofFrontiers in immunology · 2026Article
- Post-Translational Modifications of Proteins of Malaria Parasites during the Life Cycle.International journal of molecular sciences · 2024Review
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hemozoin (HZ), the malaria pigment, is associated with the disease when released during the pro-inflammatory blood stage and co-infections with bacteria lead to a more severe disease progression. The underlying mechanisms are poorly understood and, here, we show that the impact of co-exposure to HZ and lipopolysaccharide (LPS) on monocyte-derived dendritic cells (moDC) alters the early transcriptional response to a subset of IFNγ controlled genes, HLA-DR, and PD-L1. HZ-exposure had no effect on inflammatory genes, which were substantially induced by LPS. The reduced expression of HLA-DR and PD-L1 by HZ was associated with the chromatin remodeling complex NuRD and a decreased binding of the NF-κB transcription factor RELA compared to cells stimulated with LPS alone. NuRD replaced the SWI/SNF complex variant PBAF at the specific promoters, without chromatin accessibility changes. The immune modulatory effect of HZ may lead to changed immune responses to bacterial co-infections.
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Registered trials
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