Generation of pathogenic TH17 cells in the absence of TGF-β signalling

Kamran Ghoreschi (), Arian Laurence, Xiang-Ping Yang, Cristina M. Tato, Mandy J. McGeachy, Joanne E. Konkel, Haydeé L. Ramos, Lai Wei, Todd S. Davidson, Nicolas Bouladoux, John R. Grainger, Qian Chen, Yuka Kanno, Wendy T. Watford, Hong-Wei Sun, Gérard Eberl, Ethan M. Shevach, Yasmine Belkaid, Daniel J. Cua, WanJun Chen and John J. O’Shea ()
Additional contact information
Kamran Ghoreschi: Molecular Immunology and Inflammation Branch, National Institute of Arthritis, Musculoskeletal and Skin Diseases, National Institutes of Health
Arian Laurence: Molecular Immunology and Inflammation Branch, National Institute of Arthritis, Musculoskeletal and Skin Diseases, National Institutes of Health
Xiang-Ping Yang: Molecular Immunology and Inflammation Branch, National Institute of Arthritis, Musculoskeletal and Skin Diseases, National Institutes of Health
Cristina M. Tato: Merck Research Laboratories
Mandy J. McGeachy: Merck Research Laboratories
Joanne E. Konkel: Mucosal Immunology Unit, Oral Infection and Immunity Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health
Haydeé L. Ramos: Molecular Immunology and Inflammation Branch, National Institute of Arthritis, Musculoskeletal and Skin Diseases, National Institutes of Health
Lai Wei: Molecular Immunology and Inflammation Branch, National Institute of Arthritis, Musculoskeletal and Skin Diseases, National Institutes of Health
Todd S. Davidson: Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health
Nicolas Bouladoux: Mucosal Immunology Unit, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health
John R. Grainger: Mucosal Immunology Unit, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health
Qian Chen: Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health
Yuka Kanno: Molecular Immunology and Inflammation Branch, National Institute of Arthritis, Musculoskeletal and Skin Diseases, National Institutes of Health
Wendy T. Watford: Molecular Immunology and Inflammation Branch, National Institute of Arthritis, Musculoskeletal and Skin Diseases, National Institutes of Health
Hong-Wei Sun: Biodata Mining and Discovery Section, National Institute of Arthritis, Musculoskeletal and Skin Diseases, National Institutes of Health
Gérard Eberl: Institut Pasteur
Ethan M. Shevach: Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health
Yasmine Belkaid: Mucosal Immunology Unit, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health
Daniel J. Cua: Merck Research Laboratories
WanJun Chen: Mucosal Immunology Unit, Oral Infection and Immunity Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health
John J. O’Shea: Molecular Immunology and Inflammation Branch, National Institute of Arthritis, Musculoskeletal and Skin Diseases, National Institutes of Health

Nature, 2010, vol. 467, issue 7318, 967-971

Abstract: Alternative route to TH17 cells T-helper 17 (TH17) cells are a subset of T-helper cells that produce interleukin (IL)-17 and are critical for host immunity. IL-6 and transforming growth factor-β (TGF-β) had been thought of as the principal inducers of TH17 differentiation, but this work provides further support for an alternative TGF-β-independent pathway of TH17 cell differentiation in mice. TH17 cells can be generated in the absence of TGF-β signalling by using IL-23 in combination with IL-6 and IL-1β. The resulting TH17 cells express not only RORγ-t, but also T-bet, and are more pathogenic than TH17 cells generated in the presence of TGF-β. These TH17 cells, generated independently of TGF-β, could be potential targets for the treatment of autoimmune disease.

Date: 2010
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DOI: 10.1038/nature09447

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