Nature Communications (Nov 2017)
Transcriptional signature of human pro-inflammatory TH17 cells identifies reduced IL10 gene expression in multiple sclerosis
- Dan Hu,
- Samuele Notarbartolo,
- Tom Croonenborghs,
- Bonny Patel,
- Ron Cialic,
- Tun-Hsiang Yang,
- Dominik Aschenbrenner,
- Karin M. Andersson,
- Marco Gattorno,
- Minh Pham,
- Pia Kivisakk,
- Isabelle V. Pierre,
- Youjin Lee,
- Karun Kiani,
- Maria Bokarewa,
- Emily Tjon,
- Nathalie Pochet,
- Federica Sallusto,
- Vijay K. Kuchroo,
- Howard L. Weiner
Affiliations
- Dan Hu
- Ann Romney Center for Neurologic Diseases and Evergrande Center for Immunologic Diseases, Brigham and Women’s Hospital, Harvard Medical School
- Samuele Notarbartolo
- Institute for Research in Biomedicine, Università della Svizzera italiana
- Tom Croonenborghs
- Program in Translational NeuroPsychiatric Genomics, Brigham and Women’s Hospital, Harvard Medical School
- Bonny Patel
- Ann Romney Center for Neurologic Diseases and Evergrande Center for Immunologic Diseases, Brigham and Women’s Hospital, Harvard Medical School
- Ron Cialic
- Ann Romney Center for Neurologic Diseases and Evergrande Center for Immunologic Diseases, Brigham and Women’s Hospital, Harvard Medical School
- Tun-Hsiang Yang
- Department of Genetics, Harvard Medical School
- Dominik Aschenbrenner
- Institute for Research in Biomedicine, Università della Svizzera italiana
- Karin M. Andersson
- Department of Rheumatology and Inflammation Research, Sahlgrenska University Hospital, Gothenburg University
- Marco Gattorno
- Second Division of Pediatrics, G. Gaslini Scientific Institute
- Minh Pham
- Ann Romney Center for Neurologic Diseases and Evergrande Center for Immunologic Diseases, Brigham and Women’s Hospital, Harvard Medical School
- Pia Kivisakk
- Ann Romney Center for Neurologic Diseases and Evergrande Center for Immunologic Diseases, Brigham and Women’s Hospital, Harvard Medical School
- Isabelle V. Pierre
- Ann Romney Center for Neurologic Diseases and Evergrande Center for Immunologic Diseases, Brigham and Women’s Hospital, Harvard Medical School
- Youjin Lee
- Ann Romney Center for Neurologic Diseases and Evergrande Center for Immunologic Diseases, Brigham and Women’s Hospital, Harvard Medical School
- Karun Kiani
- Program in Translational NeuroPsychiatric Genomics, Brigham and Women’s Hospital, Harvard Medical School
- Maria Bokarewa
- Department of Rheumatology and Inflammation Research, Sahlgrenska University Hospital, Gothenburg University
- Emily Tjon
- Ann Romney Center for Neurologic Diseases and Evergrande Center for Immunologic Diseases, Brigham and Women’s Hospital, Harvard Medical School
- Nathalie Pochet
- Program in Translational NeuroPsychiatric Genomics, Brigham and Women’s Hospital, Harvard Medical School
- Federica Sallusto
- Institute for Research in Biomedicine, Università della Svizzera italiana
- Vijay K. Kuchroo
- Ann Romney Center for Neurologic Diseases and Evergrande Center for Immunologic Diseases, Brigham and Women’s Hospital, Harvard Medical School
- Howard L. Weiner
- Ann Romney Center for Neurologic Diseases and Evergrande Center for Immunologic Diseases, Brigham and Women’s Hospital, Harvard Medical School
- DOI
- https://doi.org/10.1038/s41467-017-01571-8
- Journal volume & issue
-
Vol. 8,
no. 1
pp. 1 – 14
Abstract
CD4+ T cells secreting interleukin-17 (TH17) have diverse functions in modulating autoimmune diseases. Here the authors show via transcriptome analyses that a subset of human TH 17 co-expressing interferon-γ (TH1/17) has a molecular signature similar to “pathogenic” mouse TH 17 but distinct from “non-pathogenic” mouse TH 17.
