Q586B2 is a crucial virulence factor during the early stages of Trypanosoma brucei infection that is conserved amongst trypanosomatids

Benoit Stijlemans (), Patrick Baetselier, Inge Molle, Laurence Lecordier, Erika Hendrickx, Ema Romão, Cécile Vincke, Wendy Baetens, Steve Schoonooghe, Gholamreza Hassanzadeh-Ghassabeh, Hannelie Korf, Marie Wallays, Joar E. Pinto Torres, David Perez-Morga, Lea Brys, Oscar Campetella, María S. Leguizamón, Mathieu Claes, Sarah Hendrickx, Dorien Mabille, Guy Caljon, Han Remaut, Kim Roelants, Stefan Magez, Jo A. Ginderachter and Carl Trez
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Benoit Stijlemans: Vrije Universiteit Brussel
Patrick Baetselier: Vrije Universiteit Brussel
Inge Molle: Vrije Universiteit Brussel
Laurence Lecordier: Université Libre de Bruxelles
Erika Hendrickx: IBMM, Université Libre de Bruxelles
Ema Romão: Vrije Universiteit Brussel
Cécile Vincke: Vrije Universiteit Brussel
Wendy Baetens: Vrije Universiteit Brussel
Steve Schoonooghe: Vrije Universiteit Brussel
Gholamreza Hassanzadeh-Ghassabeh: Vrije Universiteit Brussel
Hannelie Korf: KU Leuven
Marie Wallays: KU Leuven
Joar E. Pinto Torres: Vrije Universiteit Brussel
David Perez-Morga: IBMM, Université Libre de Bruxelles
Lea Brys: Vrije Universiteit Brussel
Oscar Campetella: Universidad Nacional de San Martín-CONICET
María S. Leguizamón: Universidad Nacional de San Martín-CONICET
Mathieu Claes: University of Antwerp
Sarah Hendrickx: University of Antwerp
Dorien Mabille: University of Antwerp
Guy Caljon: University of Antwerp
Han Remaut: Vrije Universiteit Brussel
Kim Roelants: Vrije Universiteit Brussel
Stefan Magez: Vrije Universiteit Brussel
Jo A. Ginderachter: Vrije Universiteit Brussel
Carl Trez: Vrije Universiteit Brussel

Nature Communications, 2024, vol. 15, issue 1, 1-18

Abstract: Abstract Human African trypanosomiasis or sleeping sickness, caused by the protozoan parasite Trypanosoma brucei, is characterized by the manipulation of the host’s immune response to ensure parasite invasion and persistence. Uncovering key molecules that support parasite establishment is a prerequisite to interfere with this process. We identified Q586B2 as a T. brucei protein that induces IL-10 in myeloid cells, which promotes parasite infection invasiveness. Q586B2 is expressed during all T. brucei life stages and is conserved in all Trypanosomatidae. Deleting the Q586B2-encoding Tb927.6.4140 gene in T. brucei results in a decreased peak parasitemia and prolonged survival, without affecting parasite fitness in vitro, yet promoting short stumpy differentiation in vivo. Accordingly, neutralization of Q586B2 with newly generated nanobodies could hamper myeloid-derived IL-10 production and reduce parasitemia. In addition, immunization with Q586B2 delays mortality upon a challenge with various trypanosomes, including Trypanosoma cruzi. Collectively, we uncovered a conserved protein playing an important regulatory role in Trypanosomatid infection establishment.

Date: 2024
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DOI: 10.1038/s41467-024-46067-4

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