Engineered IL-10 variants elicit potent immunomodulatory effects at low ligand doses.


Journal

Science signaling
ISSN: 1937-9145
Titre abrégé: Sci Signal
Pays: United States
ID NLM: 101465400

Informations de publication

Date de publication:
15 09 2020
Historique:
entrez: 16 9 2020
pubmed: 17 9 2020
medline: 30 10 2021
Statut: epublish

Résumé

Interleukin-10 (IL-10) is a dimeric cytokine with both immunosuppressive and immunostimulatory activities; however, IL-10-based therapies have shown only marginal clinical benefits. Here, we explored whether the stability of the IL-10 receptor complex contributes to the immunomodulatory potency of IL-10. We generated an IL-10 mutant with enhanced affinity for its IL-10Rβ receptor using yeast surface display. Compared to the wild-type cytokine, the affinity-enhanced IL-10 variants recruited IL-10Rβ more efficiently into active cell surface signaling complexes and triggered greater STAT1 and STAT3 activation in human monocytes and CD8

Identifiants

pubmed: 32934073
pii: 13/649/eabc0653
doi: 10.1126/scisignal.abc0653
pmc: PMC7685028
mid: NIHMS1636869
pii:
doi:

Substances chimiques

Ligands 0
Receptors, Interleukin-10 0
STAT1 Transcription Factor 0
STAT1 protein, human 0
STAT3 Transcription Factor 0
STAT3 protein, human 0
Interleukin-10 130068-27-8

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : Wellcome Trust
Pays : United Kingdom
Organisme : NIAID NIH HHS
ID : R01 AI097629
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI143554
Pays : United States
Organisme : Wellcome Trust
ID : 202323/Z/16/Z
Pays : United Kingdom
Organisme : Wellcome Trust
ID : 203752/Z/16/Z
Pays : United Kingdom

Informations de copyright

Copyright © 2020 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.

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Auteurs

Claire Gorby (C)

Division of Cell Signalling and Immunology, School of Life Sciences, University of Dundee, Dundee DD15EH, UK.

Junel Sotolongo Bellón (J)

Department of Biology and Center for Cellular Nanoanalytics (CellNanOs), University of Osnabrück, Barbarastraße 11, 49076 Osnabrück, Germany.

Stephan Wilmes (S)

Division of Cell Signalling and Immunology, School of Life Sciences, University of Dundee, Dundee DD15EH, UK.

Walid Warda (W)

Université Bourgogne Franche-Comté, INSERM, EFS BFC, UMR1098, RIGHT Interactions Greffon-Hôte-Tumeur/Ingénierie Cellulaire et Génique, F-25000 Besançon, France.

Elizabeth Pohler (E)

Division of Cell Signalling and Immunology, School of Life Sciences, University of Dundee, Dundee DD15EH, UK.

Paul K Fyfe (PK)

Division of Cell Signalling and Immunology, School of Life Sciences, University of Dundee, Dundee DD15EH, UK.

Adeline Cozzani (A)

Université de Lille, INSERM UMR1277 CNRS UMR9020-CANTHER and Institut pour la Recherche sur le Cancer de Lille (IRCL), Lille, France.

Christophe Ferrand (C)

Université Bourgogne Franche-Comté, INSERM, EFS BFC, UMR1098, RIGHT Interactions Greffon-Hôte-Tumeur/Ingénierie Cellulaire et Génique, F-25000 Besançon, France.

Mark R Walter (MR)

Department of Microbiology, University of Alabama at Birmingham, Birmingham, AL 35243, USA.

Suman Mitra (S)

Université de Lille, INSERM UMR1277 CNRS UMR9020-CANTHER and Institut pour la Recherche sur le Cancer de Lille (IRCL), Lille, France.

Jacob Piehler (J)

Department of Biology and Center for Cellular Nanoanalytics (CellNanOs), University of Osnabrück, Barbarastraße 11, 49076 Osnabrück, Germany.

Ignacio Moraga (I)

Division of Cell Signalling and Immunology, School of Life Sciences, University of Dundee, Dundee DD15EH, UK. imoragagonzalez@dundee.ac.uk.

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Classifications MeSH