RORγt drives production of the cytokine GM-CSF in helper T cells, which is essential for the effector phase of autoimmune ... View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2011-06

AUTHORS

Laura Codarri, Gabor Gyülvészi, Vinko Tosevski, Lysann Hesske, Adriano Fontana, Laurent Magnenat, Tobias Suter, Burkhard Becher

ABSTRACT

Although the role of the T(H)1 and T(H)17 subsets of helper T cells as disease mediators in autoimmune neuroinflammation remains a subject of some debate, none of their signature cytokines are essential for disease development. Here we report that interleukin 23 (IL-23) and the transcription factor RORγt drove expression of the cytokine GM-CSF in helper T cells, whereas IL-12, interferon-γ (IFN-γ) and IL-27 acted as negative regulators. Autoreactive helper T cells specifically lacking GM-CSF failed to initiate neuroinflammation despite expression of IL-17A or IFN-γ, whereas GM-CSF secretion by Ifng(-/-)Il17a(-/-) helper T cells was sufficient to induce experimental autoimmune encephalomyelitis (EAE). During the disease effector phase, GM-CSF sustained neuroinflammation via myeloid cells that infiltrated the central nervous system. Thus, in contrast to all other known helper T cell-derived cytokines, GM-CSF serves a nonredundant function in the initiation of autoimmune inflammation regardless of helper T cell polarization. More... »

PAGES

560

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/ni.2027

DOI

http://dx.doi.org/10.1038/ni.2027

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1040018473

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/21516112


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