IDEAS home Printed from https://ideas.repec.org/a/nat/nature/v467y2010i7318d10.1038_nature09447.html
   My bibliography  Save this article

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

Author

Listed:
  • 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)

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.

Suggested Citation

  • 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 & Qi, 2010. "Generation of pathogenic TH17 cells in the absence of TGF-β signalling," Nature, Nature, vol. 467(7318), pages 967-971, October.
    • Handle: RePEc:nat:nature:v:467:y:2010:i:7318:d:10.1038_nature09447
    DOI: 10.1038/nature09447
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/nature09447
    File Function: Abstract
    Download Restriction: Access to the full text of the articles in this series is restricted.
    File URL: https://libkey.io/10.1038/nature09447?utm_source=ideas
    LibKey link: if access is restricted and if your library uses this service, LibKey will redirect you to where you can use your library subscription to access this item
    ---><---

    As the access to this document is restricted, you may want to search for a different version of it.

    Citations

    Citations are extracted by the CitEc Project, subscribe to its RSS feed for this item.
    as


    Cited by:

    1. Lin Du & Bo Man Ho & Linbin Zhou & Yolanda Wong Ying Yip & Jing Na He & Yingying Wei & Clement C. Tham & Sun On Chan & Andrew V. Schally & Chi Pui Pang & Jian Li & Wai Kit Chu, 2023. "Growth hormone releasing hormone signaling promotes Th17 cell differentiation and autoimmune inflammation," Nature Communications, Nature, vol. 14(1), pages 1-15, December.
    2. Byung Jo Choi & Min Hee Park & Kang Ho Park & Wan Hui Han & Hee Ji Yoon & Hye Yoon Jung & Ju Yeon Hong & Md Riad Chowdhury & Kyung Yeol Kim & Jihoon Lee & Im-Sook Song & Minyeong Pang & Min-Koo Choi &, 2023. "Immunotherapy targeting plasma ASM is protective in a mouse model of Alzheimer’s disease," Nature Communications, Nature, vol. 14(1), pages 1-17, December.

    More about this item

    Statistics

    Access and download statistics

    Corrections

    All material on this site has been provided by the respective publishers and authors. You can help correct errors and omissions. When requesting a correction, please mention this item's handle: RePEc:nat:nature:v:467:y:2010:i:7318:d:10.1038_nature09447. See general information about how to correct material in RePEc.

    If you have authored this item and are not yet registered with RePEc, we encourage you to do it here. This allows to link your profile to this item. It also allows you to accept potential citations to this item that we are uncertain about.

    We have no bibliographic references for this item. You can help adding them by using this form .

    If you know of missing items citing this one, you can help us creating those links by adding the relevant references in the same way as above, for each refering item. If you are a registered author of this item, you may also want to check the "citations" tab in your RePEc Author Service profile, as there may be some citations waiting for confirmation.

    For technical questions regarding this item, or to correct its authors, title, abstract, bibliographic or download information, contact: Sonal Shukla or Springer Nature Abstracting and Indexing (email available below). General contact details of provider: http://www.nature.com .

    Please note that corrections may take a couple of weeks to filter through the various RePEc services.

    IDEAS is a RePEc service. RePEc uses bibliographic data supplied by the respective publishers.