ArticleEuropean journal of immunology2019
Macrophages assemble! But do they need IL-4R during schistosomiasis?
Article in European journal of immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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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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
7 citing papers in PubMed, 9 citations in OpenAlex.
- Primed mesenchymal stem cells attenuate schistosomiasis fibrosis by enhancing macrophage subset switching and efferocytosis via Itgb2-Rac1 axis.Cell death discovery · 2026Article
- Schistosome egg-derived extracellular vesicles deliver Sja-miR-71a inhibits host macrophage and neutrophil extracellular traps via targeting Sema4D.Cell communication and signaling : CCS · 2023Article
- Immunological mechanisms involved in macrophage activation and polarization in schistosomiasis.Parasitology · 2023Review
- CD18 controls the development and activation of monocyte-to-macrophage axis during chronic schistosomiasis.Frontiers in immunology · 2022Article
- Ongoing Exposure to Peritoneal Dialysis Fluid Alters Resident Peritoneal Macrophage Phenotype and Activation Propensity.Frontiers in immunology · 2021Article
- Monocyte and Macrophage-Mediated Pathology and Protective Immunity During Schistosomiasis.Frontiers in microbiology · 2020Review
- A Dual Role for Macrophages in Modulating Lung Tissue Damage/Repair during L2Pathogens (Basel, Switzerland) · 2019Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Helminth infections are a global health burden in humans and livestock and are considered to be a major evolutionary driver of type 2 immunity (orchestrated by type 2 cytokines, e.g., IL-4 and IL-13). Upon infection, helminths cause substantial damage to mucosal tissues as they migrate within the host and elicit crucial protective immune mechanisms. Macrophages, essential innate cells, are known to adopt a specific activation status (termed M(IL-4)) in type 2 cytokine environments. Yet, the role of these macrophages in mediating protective immune/wound healing responses to helminths is unclear. Furthermore, macrophage subsets can be very heterogenous (linked to their differing cellular origins) and the relative role of these subsets in the context of M(IL-4) activation to helminth infection is unknown. An article by Rolot et al. in this issue of the European Journal of Immunology [Eur. J. Immunol. 2019. 49: 1067-1081] uses a variety of transgenic murine strains to revise our understanding of the complexity of how these subsets undergo M(IL-4) activation and participate in wound healing responses in helminth infection. Here we highlight that consideration of different macrophage subsets in mucosal tissues is essential when evaluating the functional role of M(IL-4) macrophages.
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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 OpenQuestion graph.