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Showing 1–7 of 7 results
Advanced filters: Author: Laurence Lecordier Clear advanced filters

  • Decreased functionality and expression of trypanosome haptoglobin-hemoglobin receptor (HpHbR) is one of the evolutionary modifications that have allowed Trypanosoma brucei gambiense to infect humans. Here, Horakova et al. show that hemoglobin uptake in African trypanosomes is mediated almost exclusively by HpHbR and relevant for slender-to-stumpy differentiation. T. b. gambiense is poorly competent to differentiate into stumpy forms compared to T. b. brucei, due to reduced functionality of HpHbR.

    • Eva Horáková
    • Laurence Lecordier
    • Julius Lukeš
    ResearchOpen Access
    Nature Communications
    Volume: 13, P: 1-14

  • Sleeping sickness caused by African trypanosome parasites induces a chronic, and potentially lethal, infection in humans. Here, the authors uncover a conserved protein, Q586B2, playing an important regulatory role in Trypanosomatid infection establishment.

    • Benoit Stijlemans
    • Patrick De Baetselier
    • Carl De Trez
    ResearchOpen Access
    Nature Communications
    Volume: 15, P: 1-18

  • The human serum protein apolipoprotein L1 (APOL1) is taken up by trypanosomes where it triggers cell death, forming pores in endolysosomal membranes. Vanwalleghem et al.show that APOL1 triggers both lysosomal and mitochondrial membrane permeabilization, and that the latter is responsible for trypanolysis.

    • Gilles Vanwalleghem
    • Frédéric Fontaine
    • Etienne Pays
    ResearchOpen Access
    Nature Communications
    Volume: 6, P: 1-10

  • Recombinant proteins based on APOL1 and APOL3 can kill pathogenic Trypanosoma brucei subspecies, including a variant (rPpMUT) that is effective against T.b. gambiense infection in mice, suggesting that it may serve as a therapy against sleeping sickness.

    • Frédéric Fontaine
    • Laurence Lecordier
    • Etienne Pays
    Research
    Nature Microbiology
    Volume: 2, P: 1500-1506

  • This study shows that Trypanosoma brucei gambiense resists trypanolytic factors (TLFs) in a multifactorial manner, relying on a hydrophobic β-sheet of the TgsGP glycoprotein, which prevents APOL1 toxicity and induces membrane stiffening, as well as a reduction in sensitivity to APOL1 requiring cysteine protease activity and TLF-1 receptor inactivation owing to a single amino acid substitution.

    • Pierrick Uzureau
    • Sophie Uzureau
    • Etienne Pays
    Research
    Nature
    Volume: 501, P: 430-434

  • Humans can resist infection by African trypanosomes, owing to the trypanolytic activity of apolipoprotein L1 (APOL1), which is associated with two serum complexes, trypanosome lytic factor 1 (TLF1) and TFL2.Trypanosoma brucei rhodesiense and Trypanosoma brucei gambiense evade this defence mechanism by expressing resistance proteins and in turn, populations in western Africa can restore resistance to T. b. rhodesiense via sequence variation in APOL1. Pays et. al. review this complex relationship and its evolutionary importance.

    • Etienne Pays
    • Benoit Vanhollebeke
    • David Pérez-Morga
    Reviews
    Nature Reviews Microbiology
    Volume: 12, P: 575-584