ArticleExperimental parasitology2008
Low levels of mammalian TGF-beta1 are protective against malaria parasite infection, a paradox clarified in the mosquito host.
Article in Experimental parasitology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 13 citations in OpenAlex.
- Influence of blood feeding and infection on arthropod hemocytes.Current opinion in insect science · 2025Review
- Article
- Transcriptional Modulation of the Host Immunity Mediated by Cytokines and Transcriptional Factors inBiomolecules · 2019Article
- In vivo, in vitro, and in silico studies suggest a conserved immune module that regulates malaria parasite transmission from mammals to mosquitoes.Journal of theoretical biology · 2013Article
- Human host-derived cytokines associated with Plasmodium vivax transmission from acute malaria patients to Anopheles darlingi mosquitoes in the Peruvian Amazon.The American journal of tropical medicine and hygiene · 2013Article
- Sustained activation of Akt elicits mitochondrial dysfunction to block Plasmodium falciparum infection in the mosquito host.PLoS pathogens · 2013Article
- Translational systems approaches to the biology of inflammation and healing.Immunopharmacology and immunotoxicology · 2010Review
- MAPK ERK signaling regulates the TGF-beta1-dependent mosquito response to Plasmodium falciparum.PLoS pathogens · 2009Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Nitric oxide (NO), derived from catalysis of inducible NO synthase (iNOS), limits malaria parasite growth in mammals. Transforming growth factor (TGF)-beta1 suppresses iNOS in cells in vitro as well as in vivo in mice, but paradoxically severe malaria in humans is associated with low levels of TGF-beta1. We hypothesized that this paradox is a universal feature of infection and occurs in the mosquito Anopheles stephensi, an invertebrate host for Plasmodium that also regulates parasite development with inducible NO synthase (AsNOS). We show that exogenous human TGF-beta1 dose-dependently regulates mosquito AsNOS expression and that parasite killing by low dose TGF-beta1 depends on AsNOS catalysis. Furthermore, induction of AsNOS expression by TGF-beta1 is regulated by NO synthesis. These results suggest that TGF-beta1 plays similar roles during parasite infection in mammals and mosquitoes and that this role is linked to the effects of TGF-beta1 on inducible NO synthesis.
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