Nature Communications (Jan 2019)
RORγt inhibition selectively targets IL-17 producing iNKT and γδ-T cells enriched in Spondyloarthritis patients
- Koen Venken,
- Peggy Jacques,
- Céline Mortier,
- Mark E. Labadia,
- Tine Decruy,
- Julie Coudenys,
- Kathleen Hoyt,
- Anita L. Wayne,
- Robert Hughes,
- Michael Turner,
- Sofie Van Gassen,
- Liesbet Martens,
- Dustin Smith,
- Christian Harcken,
- Joseph Wahle,
- Chao-Ting Wang,
- Eveline Verheugen,
- Nadia Schryvers,
- Gaëlle Varkas,
- Heleen Cypers,
- Ruth Wittoek,
- Yves Piette,
- Lieve Gyselbrecht,
- Serge Van Calenbergh,
- Filip Van den Bosch,
- Yvan Saeys,
- Gerald Nabozny,
- Dirk Elewaut
Affiliations
- Koen Venken
- Department of Rheumatology, Faculty of Medicine and Health Sciences, Laboratory for Molecular Immunology and Inflammation, Ghent University
- Peggy Jacques
- Department of Rheumatology, Faculty of Medicine and Health Sciences, Laboratory for Molecular Immunology and Inflammation, Ghent University
- Céline Mortier
- Department of Rheumatology, Faculty of Medicine and Health Sciences, Laboratory for Molecular Immunology and Inflammation, Ghent University
- Mark E. Labadia
- Research and Development Boehringer-Ingelheim
- Tine Decruy
- Department of Rheumatology, Faculty of Medicine and Health Sciences, Laboratory for Molecular Immunology and Inflammation, Ghent University
- Julie Coudenys
- Department of Rheumatology, Faculty of Medicine and Health Sciences, Laboratory for Molecular Immunology and Inflammation, Ghent University
- Kathleen Hoyt
- Research and Development Boehringer-Ingelheim
- Anita L. Wayne
- Research and Development Boehringer-Ingelheim
- Robert Hughes
- Research and Development Boehringer-Ingelheim
- Michael Turner
- Research and Development Boehringer-Ingelheim
- Sofie Van Gassen
- VIB Inflammation Research Center, Ghent University
- Liesbet Martens
- VIB Inflammation Research Center, Ghent University
- Dustin Smith
- Research and Development Boehringer-Ingelheim
- Christian Harcken
- Research and Development Boehringer-Ingelheim
- Joseph Wahle
- Research and Development Boehringer-Ingelheim
- Chao-Ting Wang
- Research and Development Boehringer-Ingelheim
- Eveline Verheugen
- Department of Rheumatology, Faculty of Medicine and Health Sciences, Laboratory for Molecular Immunology and Inflammation, Ghent University
- Nadia Schryvers
- Department of Rheumatology, Faculty of Medicine and Health Sciences, Laboratory for Molecular Immunology and Inflammation, Ghent University
- Gaëlle Varkas
- Department of Rheumatology, Faculty of Medicine and Health Sciences, Laboratory for Molecular Immunology and Inflammation, Ghent University
- Heleen Cypers
- Department of Rheumatology, Faculty of Medicine and Health Sciences, Laboratory for Molecular Immunology and Inflammation, Ghent University
- Ruth Wittoek
- Department of Rheumatology, Faculty of Medicine and Health Sciences, Laboratory for Molecular Immunology and Inflammation, Ghent University
- Yves Piette
- Department of Rheumatology, Faculty of Medicine and Health Sciences, Laboratory for Molecular Immunology and Inflammation, Ghent University
- Lieve Gyselbrecht
- ASZ Aalst
- Serge Van Calenbergh
- Laboratory for Medicinal Chemistry, Faculty of Pharmaceutical Sciences, Ghent University
- Filip Van den Bosch
- Department of Rheumatology, Faculty of Medicine and Health Sciences, Laboratory for Molecular Immunology and Inflammation, Ghent University
- Yvan Saeys
- VIB Inflammation Research Center, Ghent University
- Gerald Nabozny
- Research and Development Boehringer-Ingelheim
- Dirk Elewaut
- Department of Rheumatology, Faculty of Medicine and Health Sciences, Laboratory for Molecular Immunology and Inflammation, Ghent University
- DOI
- https://doi.org/10.1038/s41467-018-07911-6
- Journal volume & issue
-
Vol. 10,
no. 1
pp. 1 – 15
Abstract
The role of innate T cell subsets in the pathogenesis of spondyloarthritis (SpA) is not well understood. Here, the authors examine the role of invariant natural killer T (iNKT) and γδ-T cells in SpA and show that disease-derived iNKT and γδ-T cells have unique and Th17-skewed phenotype and gene expression profiles within inflamed joints.
