A structurally distinct TGF-β mimic from an intestinal helminth parasite potently induces regulatory T cells

Chris J. C. Johnston, Danielle J. Smyth, Ravindra B. Kodali, Madeleine P. J. White, Yvonne Harcus, Kara J. Filbey, James P. Hewitson, Cynthia S. Hinck, Alasdair Ivens, Andrea M. Kemter, Anna O. Kildemoes, Thierry Bihan, Dinesh C. Soares, Stephen M. Anderton, Thomas Brenn, Stephen J. Wigmore, Hannah V. Woodcock, Rachel C. Chambers, Andrew P. Hinck, Henry J. McSorley and Rick M. Maizels ()
Additional contact information
Chris J. C. Johnston: University of Edinburgh
Danielle J. Smyth: University of Edinburgh
Ravindra B. Kodali: University of Pittsburgh School of Medicine
Madeleine P. J. White: University of Glasgow
Yvonne Harcus: University of Edinburgh
Kara J. Filbey: University of Edinburgh
James P. Hewitson: University of Edinburgh
Cynthia S. Hinck: University of Pittsburgh School of Medicine
Alasdair Ivens: University of Edinburgh
Andrea M. Kemter: University of Edinburgh
Anna O. Kildemoes: University of Edinburgh
Thierry Bihan: University of Edinburgh
Dinesh C. Soares: University of Edinburgh
Stephen M. Anderton: University of Edinburgh
Thomas Brenn: University of Edinburgh
Stephen J. Wigmore: University of Edinburgh
Hannah V. Woodcock: University College London
Rachel C. Chambers: University College London
Andrew P. Hinck: University of Pittsburgh School of Medicine
Henry J. McSorley: University of Edinburgh
Rick M. Maizels: University of Glasgow

Nature Communications, 2017, vol. 8, issue 1, 1-13

Abstract: Abstract Helminth parasites defy immune exclusion through sophisticated evasion mechanisms, including activation of host immunosuppressive regulatory T (Treg) cells. The mouse parasite Heligmosomoides polygyrus can expand the host Treg population by secreting products that activate TGF-β signalling, but the identity of the active molecule is unknown. Here we identify an H. polygyrus TGF-β mimic (Hp-TGM) that replicates the biological and functional properties of TGF-β, including binding to mammalian TGF-β receptors and inducing mouse and human Foxp3+ Treg cells. Hp-TGM has no homology with mammalian TGF-β or other members of the TGF-β family, but is a member of the complement control protein superfamily. Thus, our data indicate that through convergent evolution, the parasite has acquired a protein with cytokine-like function that is able to exploit an endogenous pathway of immunoregulation in the host.

Date: 2017
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DOI: 10.1038/s41467-017-01886-6

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