ArticleThe Journal of experimental medicine2003
Activation of transforming growth factor beta by malaria parasite-derived metalloproteinases and a thrombospondin-like molecule.
Article in The Journal of experimental medicine, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.
- Pooled it
- Baseline Treg frequency, Treg-associated immune checkpoint responses, and plasma IL-10 responses during controlled human malaria infection in semi-immune Kenyan adults: a secondary analysis of the CHMI-SIKA Study.The Lancet. Microbe · 2026Article
- Thrombocytopenia in patients with Plasmodium vivax in Colombia is associated with anti-phosphatidylserine autoantibodies and IL-6, IFNγ, IL-10 and TGF-β.PLoS neglected tropical diseases · 2025Article
- Microvascular significance of TGF-β axis activation in COVID-19.Frontiers in cardiovascular medicine · 2022Review
- Immunosuppression in Malaria: DoPathogens (Basel, Switzerland) · 2021Review
- The parasite cytokine mimic Hp-TGM potently replicates the regulatory effects of TGF-β on murine CD4Immunology and cell biology · 2021Article
- Identification of chlorophyll a-b binding protein AB96 as a novel TGFβ1 neutralizing agent.Scientific reports · 2021Article
- Balancing in a black box: Potential immunomodulatory roles for TGF-β signaling during blood-stage malaria.Virulence · 2020Review
- Using two phases of the CD4 T cell response to blood-stage murine malaria to understand regulation of systemic immunity and placental pathology in Plasmodium falciparum infection.Immunological reviews · 2020Review
- Cardiac Chagas Disease: MMPs, TIMPs, Galectins, and TGF-Disease markers · 2019Review
- A systematic and prospectively validated approach for identifying synergistic drug combinations against malaria.Malaria journal · 2018Article
- Regulation of the Immune Response by TGF-β: From Conception to Autoimmunity and Infection.Cold Spring Harbor perspectives in biology · 2017Review
- Decline of FoxP3+ Regulatory CD4 T Cells in Peripheral Blood of Children Heavily Exposed to Malaria.PLoS pathogens · 2015Article
- Article
- Article
- Mechanisms underlying the induction of regulatory T cells and its relevance in the adaptive immune response in parasitic infections.International journal of biological sciences · 2011Review
- Transforming growth factor-β: activation by neuraminidase and role in highly pathogenic H5N1 influenza pathogenesis.PLoS pathogens · 2010Article
- Immunity and immunopathology to viruses: what decides the outcome?Nature reviews. Immunology · 2010Review
- Cerebral malaria: insights from host-parasite protein-protein interactions.Malaria journal · 2010Article
- IL-10 from CD4CD25Foxp3CD127 adaptive regulatory T cells modulates parasite clearance and pathology during malaria infection.PLoS pathogens · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Much of the pathology of malaria is mediated by inflammatory cytokines (such as interleukin 12, interferon gamma, and tumor necrosis factor alpha), which are part of the immune response that kills the parasite. The antiinflammatory cytokine transforming growth factor (TGF)-beta plays a crucial role in preventing the severe pathology of malaria in mice and TGF-beta production is associated with reduced risk of clinical malaria in humans. Here we show that serum-free preparations of Plasmodium falciparum, Plasmodium yoelii 17XL, and Plasmodium berghei schizont-infected erythrocytes, but not equivalent preparations of uninfected erythrocytes, are directly able to activate latent TGF-beta (LatTGF-beta) in vitro. Antibodies to thrombospondin (TSP) and to a P. falciparum TSP-related adhesive protein (PfTRAP), and synthetic peptides from PfTRAP and P. berghei TRAP that represent homologues of TGF-beta binding motifs of TSP, all inhibit malaria-mediated TGF-beta activation. Importantly, TRAP-deficient P. berghei parasites are less able to activate LatTGF-beta than wild-type parasites and their replication is attenuated in vitro. We show that activation of TGF-beta by malaria parasites is a two step process involving TSP-like molecules and metalloproteinase activity. Activation of LatTGF-beta represents a novel mechanism for direct modulation of the host response by malaria parasites.
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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.