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Purification of Extracellular Trypanosomes, Including African, from Blood by Anion-Exchangers (Diethylaminoethyl-cellulose Columns)

Purification of Extracellular Trypanosomes, Including African, from Blood by Anion-Exchangers (Diethylaminoethyl-cellulose Columns)

Published on: April 6, 2019

Human innate immunity against African trypanosomes.

Etienne Pays¹, Benoit Vanhollebeke

¹Laboratory of Molecular Parasitology, IBMM, Université Libre de Bruxelles, 12, rue des Professeurs Jeener et Brachet, B-6041 Gosselies, Belgium.

Current Opinion in Immunology

|June 30, 2009

Summary

Human innate immunity protects against African trypanosomes via serum complexes. Apolipoprotein L-1 (apoL1) forms pores in parasites, while haptoglobin-related protein (Hpr) aids apoL1 uptake, preventing sleeping sickness.

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Area of Science:

Immunology
Parasitology
Molecular Biology

Background:

Humans possess natural resistance to Trypanosoma brucei brucei.
Only specific parasite clones evade this innate immunity, causing sleeping sickness.
Serum complexes involving apolipoprotein A-1 (apoA1), apolipoprotein L-1 (apoL1), and haptoglobin-related protein (Hpr) mediate this resistance.

Purpose of the Study:

To elucidate the distinct roles of apoL1 and Hpr in human resistance to T. brucei.
To understand the molecular mechanisms of trypanolysis mediated by these proteins.

Main Methods:

Structural and functional analysis of apoL1.
Investigation of Hpr's role in complex formation and parasite interaction.
Assessment of parasite susceptibility in the absence of Hpr or apoL1.

Main Results:

ApoL1 exhibits similarities to Bcl2 family proteins and induces trypanosome death via lysosomal membrane pore formation.
Hpr, complexed with hemoglobin (Hb), facilitates the binding of trypanolytic complexes to the parasite's Hb receptor, enhancing apoL1 internalization.
Deficiency in Hpr or apoL1 significantly reduces or eliminates human protection against T. brucei.

Conclusions:

ApoL1 and Hpr are critical components of the human innate immune defense against T. brucei.
The synergistic action of apoL1-mediated pore formation and Hpr-facilitated uptake is essential for preventing African trypanosomiasis.