Invariant surface glycoprotein 65 of Trypanosoma brucei is a complement C3 receptor

Olivia J. S. Macleod, Alexander D. Cook, Helena Webb, Mandy Crow, Roisin Burns, Maria Redpath, Stefanie Seisenberger, Camilla E. Trevor, Lori Peacock, Angela Schwede, Nicola Kimblin, Amanda F. Francisco, Julia Pepperl, Steve Rust, Paul Voorheis, Wendy Gibson, Martin C. Taylor, Matthew K. Higgins () and Mark Carrington ()
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Olivia J. S. Macleod: University of Cambridge
Alexander D. Cook: University of Oxford
Helena Webb: University of Cambridge
Mandy Crow: University of Cambridge
Roisin Burns: University of Cambridge
Maria Redpath: University of Cambridge
Stefanie Seisenberger: University of Cambridge
Camilla E. Trevor: University of Cambridge
Lori Peacock: University of Bristol
Angela Schwede: University of Cambridge
Nicola Kimblin: University of Cambridge
Amanda F. Francisco: London School of Hygiene and Tropical Medicine
Julia Pepperl: University of Cambridge
Steve Rust: Biopharmaceuticals R&D, AstraZeneca
Paul Voorheis: Trinity College Dublin
Wendy Gibson: University of Bristol
Martin C. Taylor: London School of Hygiene and Tropical Medicine
Matthew K. Higgins: University of Oxford
Mark Carrington: University of Cambridge

Nature Communications, 2022, vol. 13, issue 1, 1-10

Abstract: Abstract African trypanosomes are extracellular pathogens of mammals and are exposed to the adaptive and innate immune systems. Trypanosomes evade the adaptive immune response through antigenic variation, but little is known about how they interact with components of the innate immune response, including complement. Here we demonstrate that an invariant surface glycoprotein, ISG65, is a receptor for complement component 3 (C3). We show how ISG65 binds to the thioester domain of C3b. We also show that C3 contributes to control of trypanosomes during early infection in a mouse model and provide evidence that ISG65 is involved in reducing trypanosome susceptibility to C3-mediated clearance. Deposition of C3b on pathogen surfaces, such as trypanosomes, is a central point in activation of the complement system. In ISG65, trypanosomes have evolved a C3 receptor which diminishes the downstream effects of C3 deposition on the control of infection.

Date: 2022
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DOI: 10.1038/s41467-022-32728-9

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