ArticlePLoS pathogens2012
The receptor Slamf1 on the surface of myeloid lineage cells controls susceptibility to infection by Trypanosoma cruzi.
Article in PLoS pathogens, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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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Who cites it
22 citing papers in PubMed, 30 citations in OpenAlex.
- Towards a map of the immune system manipulation network byFrontiers in cellular and infection microbiology · 2025Review
- The immune receptors TLR4 and SLAMF1 regulate TNF release by human metapneumovirus in human macrophages.Frontiers in immunology · 2025Article
- Targeting macrophage phenotypes to prevent diseases caused byFrontiers in immunology · 2025Review
- Animal models for exploring Chagas disease pathogenesis and supporting drug discovery.Clinical microbiology reviews · 2024Review
- Quantitative Proteomic Analysis of Macrophages Infected withInternational journal of molecular sciences · 2024Article
- Immunopathogenesis inFrontiers in immunology · 2023Review
- Host-parasite dynamics in Chagas disease from systemic to hyper-local scales.Parasite immunology · 2021Review
- The Oxidative Stress and Chronic Inflammatory Process in Chagas Disease: Role of Exosomes and Contributing Genetic Factors.Oxidative medicine and cellular longevity · 2021Review
- The First Contact of Human Dendritic Cells WithFrontiers in immunology · 2021Article
- Myeloid-Derived Suppressor Cells inFrontiers in cellular and infection microbiology · 2021Review
- Interaction of Signaling Lymphocytic Activation Molecule Family 1 (SLAMF1) receptor with Trypanosoma cruzi is strain-dependent and affects NADPH oxidase expression and activity.PLoS neglected tropical diseases · 2020Article
- Genomic assemblies of newly sequenced Trypanosoma cruzi strains reveal new genomic expansion and greater complexity.Scientific reports · 2018Article
- ROS and Trypanosoma cruzi: Fuel to infection, poison to the heart.PLoS pathogens · 2018Review
- Regulatory Lymphoid and Myeloid Cells Determine the Cardiac Immunopathogenesis ofFrontiers in microbiology · 2018Review
- A multi-parametric analysis of Trypanosoma cruzi infection: common pathophysiologic patterns beyond extreme heterogeneity of host responses.Scientific reports · 2017Article
- Putting Infection Dynamics at the Heart of Chagas Disease.Trends in parasitology · 2016Review
- Host and parasite genetics shape a link between Trypanosoma cruzi infection dynamics and chronic cardiomyopathy.Cellular microbiology · 2016Article
- Dendritic Cells: A Double-Edged Sword in Immune Responses during Chagas Disease.Frontiers in microbiology · 2016Review
- Global metabolomic profiling of acute myocarditis caused by Trypanosoma cruzi infection.PLoS neglected tropical diseases · 2014Article
- Bioluminescence imaging of chronic Trypanosoma cruzi infections reveals tissue-specific parasite dynamics and heart disease in the absence of locally persistent infection.Cellular microbiology · 2014Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Trypanosoma cruzi, the protozoan parasite responsible for Chagas' disease, causes severe myocarditis often resulting in death. Here, we report that Slamf1-/- mice, which lack the hematopoietic cell surface receptor Slamf1, are completely protected from an acute lethal parasite challenge. Cardiac damage was reduced in Slamf1-/- mice compared to wild type mice, infected with the same doses of parasites, as a result of a decrease of the number of parasites in the heart even the parasitemia was only marginally less. Both in vivo and in vitro experiments reveal that Slamf1-defIcient myeloid cells are impaired in their ability to replicate the parasite and show altered production of cytokines. Importantly, IFN-γ production in the heart of Slamf1 deficient mice was much lower than in the heart of wt mice even though the number of infiltrating dendritic cells, macrophages, CD4 and CD8 T lymphocytes were comparable. Administration of an anti-Slamf1 monoclonal antibody also reduced the number of parasites and IFN-γ in the heart. These observations not only explain the reduced susceptibility to in vivo infection by the parasite, but they also suggest human Slamf1 as a potential target for therapeutic target against T. cruzi infection.
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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.