Skip Navigation


International Immunology Advance Access originally published online on December 21, 2007
International Immunology 2008 20(2):223-234; doi:10.1093/intimm/dxm139
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
20/2/223    most recent
dxm139v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (1)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Huber, M.
Right arrow Articles by Lohoff, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Huber, M.
Right arrow Articles by Lohoff, M.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?


© The Japanese Society for Immunology. 2007. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

IL-27 inhibits the development of regulatory T cells via STAT3

Magdalena Huber1, Vera Steinwald1, Anna Guralnik1, Anne Brüstle1, Peter Kleemann1, Christine Rosenplänter1, Thomas Decker2 and Michael Lohoff1

1 Institut für Medizinische Mikrobiologie und Hygiene, Universität Marburg, Hans-Meerwein-Straße 2, 35043 Marburg, Germany
2 Department für Mikrobiologie und Immunologie, Universität Wien, Dr Bohr-Gasse 9, 1030 Wien, Austria

Correspondence to: M. Huber; E-mail: huberma{at}med.uni-marburg.de

Regulatory CD4+ T cells are important for the homeostasis of the immune system and their absence correlates with autoimmune disorders. Here, we investigate the capacity of IL-27, a cytokine with pro- and anti-inflammatory properties, to regulate the generation of transforming growth factor β (TGFβ)-inducible forkhead box P3 (Foxp3)-positive regulatory T (Treg) cells. Our results demonstrate that IL-27 inhibits the acquisition of the Treg phenotype at the level of Foxp3, CD25 and CTLA-4 (CD152) expression as well as the suppressive function. In contrast to TGFβ-induced Treg cells, the cells generated after differentiation in the presence of TGFβ and IL-27 maintained the ability for IL-2 and tumour necrosis factor {alpha} (TNF{alpha}) production. The inhibitory effect of IL-27 on Treg generation was at least partially signal transducer and activator of transcription 3 (STAT3) dependent as examined by targeted STAT3 protein inhibition using small interfering RNA (siRNA), while STAT1-dependent signals seemed to oppose the STAT3 signals. In turn, TGFβ blocked IL-27-induced Th1 differentiation. Thus, IL-27 and TGFβ mutually control their effects on CD4+ T-cell differentiation, whereby IL-27 favours inflammatory conditions through a STAT3-dependent inhibition of Treg generation.

Keywords: IL-27, STAT1, STAT3, TGFβ, Treg

Transmitting editor: A. Radbruch

Received 23 October 2007, accepted 22 November 2007.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.