ArticleNature communications2023
Cryo-EM structures of Trypanosoma brucei gambiense ISG65 with human complement C3 and C3b and their roles in alternative pathway restriction.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 17 citations in OpenAlex.
- The resistance to Toxoplasma gondii in Microtus fortis is associated with the activation of the complement lectin pathway.PLoS neglected tropical diseases · 2026Article
- The grand escape - how pathogens outsmart the human complement system.Immunobiology · 2025Review
- Roles of cytokines in modulatingFrontiers in parasitology · 2025Article
- Article
- Beyond the VSG layer: Exploring the role of intrinsic disorder in the invariant surface glycoproteins of African trypanosomes.PLoS pathogens · 2024Article
- Predictive modeling and cryo-EM: A synergistic approach to modeling macromolecular structure.Biophysical journal · 2024Review
- Trypanosomes and complement: more than one way to die?Trends in parasitology · 2023Review
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Authors and funding
13 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
African Trypanosomes have developed elaborate mechanisms to escape the adaptive immune response, but little is known about complement evasion particularly at the early stage of infection. Here we show that ISG65 of the human-infective parasite Trypanosoma brucei gambiense is a receptor for human complement factor C3 and its activation fragments and that it takes over a role in selective inhibition of the alternative pathway C5 convertase and thus abrogation of the terminal pathway. No deposition of C4b, as part of the classical and lectin pathway convertases, was detected on trypanosomes. We present the cryo-electron microscopy (EM) structures of native C3 and C3b in complex with ISG65 which reveal a set of modes of complement interaction. Based on these findings, we propose a model for receptor-ligand interactions as they occur at the plasma membrane of blood-stage trypanosomes and may facilitate innate immune escape of the parasite.
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