Mechanism of resistance of African trypanosomes to cytotoxic human HDL

Kristin M. Hager and Stephen L. Hajduk
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Kristin M. Hager: University of Alabama at Birmingham, Schools of Medicine and Dentistry
Stephen L. Hajduk: University of Alabama at Birmingham, Schools of Medicine and Dentistry

Nature, 1997, vol. 385, issue 6619, 823-826

Abstract: Abstract Trypanosoma brucei brucei, the causative agent of ngana in cattle, is non-infectious to humans because of its sensitivity to the cytolytic activity of normal human serum1. The toxin in normal human serum is human haptoglobin-related protein (Hpr)2–5 which is found either as an apolipoprotein associated with a minor subclass of high-density lipoprotein (HDL), named trypanosome lytic factor (TLF1)6–8, or as an unstable, high-molecular-mass protein complex known as TLF2 (refs 5, 9–12). TLF-mediated lysis of T. b. brucei requires binding, internalization and lysosomal targeting13. The human sleeping-sickness trypanosome, Trypanosoma brucei rhodesiense is resistant to TLF. Our studies reveal that resistant trypanosomes fail to endocytose TLF yet continue to bind TLF through cell-surface receptors. On the basis of these results, we conclude that one mechanism of resistance of human sleeping-sickness trypanosomes to human serum is decreased internalization of receptor-bound TLF.

Date: 1997
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DOI: 10.1038/385823a0

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