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© Institut Pasteur
Macrophages et lymphocytes de souris. Image colorisée.
Publication : The Journal of experimental medicine

The Ets-1 transcription factor controls the development and function of natural regulatory T cells

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in The Journal of experimental medicine - 20 Sep 2010

Mouly E, Chemin K, Nguyen HV, Chopin M, Mesnard L, Leite-de-Moraes M, Burlen-defranoux O, Bandeira A, Bories JC

Link to Pubmed [PMID] – 20855499

J. Exp. Med. 2010 Sep;207(10):2113-25

Regulatory T cells (T reg cells) constitute a population of CD4(+) T cells that limits immune responses. The transcription factor Foxp3 is important for determining the development and function of T reg cells; however, the molecular mechanisms that trigger and maintain its expression remain incompletely understood. In this study, we show that mice deficient for the Ets-1 transcription factor (Ets-1(-/-)) developed T cell-mediated splenomegaly and systemic autoimmunity that can be blocked by functional wild-type T reg cells. Spleens of Ets-1(-/-) mice contained mostly activated T cells, including Th2-polarized CD4(+) cells and had reduced percentages of T reg cells. Splenic and thymic Ets-1(-/-) T reg cells expressed low levels of Foxp3 and displayed the CD103 marker that characterizes antigen-experienced T reg cells. Thymic development of Ets-1(-/-) T reg cells appeared intrinsically altered as Foxp3-expressing cells differentiate poorly in mixed fetal liver reconstituted chimera and fetal thymic organ culture. Ets-1(-/-) T reg cells showed decreased in vitro suppression activity and did not protect Rag2(-/-) hosts from naive T cell-induced inflammatory bowel disease. Furthermore, in T reg cells, Ets-1 interacted with the Foxp3 intronic enhancer and was required for demethylation of this regulatory sequence. These data demonstrate that Ets-1 is required for the development of natural T reg cells and suggest a role for this transcription factor in the regulation of Foxp3 expression.

http://www.ncbi.nlm.nih.gov/pubmed/20855499