ArticlePLoS pathogens2013
A Trypanosoma brucei kinesin heavy chain promotes parasite growth by triggering host arginase activity.
Article in PLoS pathogens, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 58 citations in OpenAlex.
- The roles of arginases and arginine in immunity.Nature reviews. Immunology · 2025Review
- Roles of cytokines in modulatingFrontiers in parasitology · 2025Article
- Differential Regulation of L-Arginine Metabolism through NOS2 and Arginases during Infection withPathogens (Basel, Switzerland) · 2024Article
- Q586B2 is a crucial virulence factor during the early stages of Trypanosoma brucei infection that is conserved amongst trypanosomatids.Nature communications · 2024Article
- Pathogenicity and virulence of African trypanosomes: From laboratory models to clinically relevant hosts.Virulence · 2023Review
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- Flow Cytometric Characterization of Macrophages InfectedBio-protocol · 2022Article
- Tipping the balance between erythroid cell differentiation and induction of anemia in response to the inflammatory pathology associated with chronic trypanosome infections.Frontiers in immunology · 2022Article
- The Role of MIF and IL-10 as Molecular Yin-Yang in the Modulation of the Host Immune Microenvironment During Infections: African Trypanosome Infections as a Paradigm.Frontiers in immunology · 2022Review
- Immunoinformatic design of a putative multi-epitope vaccine candidate againstComputational and structural biotechnology journal · 2022Article
- Genetic and immunological basis of human African trypanosomiasis.Current opinion in immunology · 2021Review
- Excreted Trypanosoma brucei proteins inhibit Plasmodium hepatic infection.PLoS neglected tropical diseases · 2021Article
- Intestinal Transcriptomic and Histologic Profiling Reveals Tissue Repair Mechanisms Underlying Resistance to the ParasitePathogens (Basel, Switzerland) · 2021Article
- African Trypanosomiasis: Extracellular Vesicles Shed byBiomedicines · 2021Article
- Article
- Role of the inhibitor of serine peptidase 2 (ISP2) of Trypanosoma brucei rhodesiense in parasite virulence and modulation of the inflammatory responses of the host.PLoS neglected tropical diseases · 2021Article
- Revisiting the Mechanisms of Immune Evasion Employed by Human Parasites.Frontiers in cellular and infection microbiology · 2021Review
- Culturing and Transfection of Pleomorphic Trypanosoma brucei.Methods in molecular biology (Clifton, N.J.) · 2020Article
- To the Skin and Beyond: The Immune Response to African Trypanosomes as They Enter and Exit the Vertebrate Host.Frontiers in immunology · 2020Review
- Overview of the role of kinetoplastid surface carbohydrates in infection and host cell invasion: prospects for therapeutic intervention.Parasitology · 2019Review
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22 authors at 11 institutions in 4 countries.
Funding
Abstract
backgroundIn order to promote infection, the blood-borne parasite Trypanosoma brucei releases factors that upregulate arginase expression and activity in myeloid cells. METHODOLOGY/PRINCIPAL
findingsBy screening a cDNA library of T. brucei with an antibody neutralizing the arginase-inducing activity of parasite released factors, we identified a Kinesin Heavy Chain isoform, termed TbKHC1, as responsible for this effect. Following interaction with mouse myeloid cells, natural or recombinant TbKHC1 triggered SIGN-R1 receptor-dependent induction of IL-10 production, resulting in arginase-1 activation concomitant with reduction of nitric oxide (NO) synthase activity. This TbKHC1 activity was IL-4Rα-independent and did not mirror M2 activation of myeloid cells. As compared to wild-type T. brucei, infection by TbKHC1 KO parasites was characterized by strongly reduced parasitaemia and prolonged host survival time. By treating infected mice with ornithine or with NO synthase inhibitor, we observed that during the first wave of parasitaemia the parasite growth-promoting effect of TbKHC1-mediated arginase activation resulted more from increased polyamine production than from reduction of NO synthesis. In late stage infection, TbKHC1-mediated reduction of NO synthesis appeared to contribute to liver damage linked to shortening of host survival time.
conclusionA kinesin heavy chain released by T. brucei induces IL-10 and arginase-1 through SIGN-R1 signaling in myeloid cells, which promotes early trypanosome growth and favors parasite settlement in the host. Moreover, in the late stage of infection, the inhibition of NO synthesis by TbKHC1 contributes to liver pathogenicity.
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