Foxo3 Transcription Factor Drives Pathogenic T Helper 1 Differentiation by Inducing the Expression of Eomes

التفاصيل البيبلوغرافية
العنوان: Foxo3 Transcription Factor Drives Pathogenic T Helper 1 Differentiation by Inducing the Expression of Eomes
المؤلفون: Stienne, Caroline, Michieletto, Michaël F, Benamar, Mehdi, Carrié, Nadège, Bernard, Isabelle, Nguyen, Xuan-Hung, Lippi, Yannick, Duguet, Fanny, Liblau, Roland S, Hedrick, Stephen M, Saoudi, Abdelhadi, Dejean, Anne S
المصدر: Immunity, vol 45, iss 4
بيانات النشر: eScholarship, University of California, 2016.
سنة النشر: 2016
مصطلحات موضوعية: CD4-Positive T-Lymphocytes, Male, Eomes, Immunology, Inbred C57BL, T-bet, Autoimmune Disease, Cell Line, Mice, Experimental, Interferon-gamma, CD4 T cell differentiation, transcription factors, Receptors, Genetics, Animals, Humans, 2.1 Biological and endogenous factors, Aetiology, Encephalomyelitis, IFN-γ, Inflammation, EAE, Inflammatory and immune system, Forkhead Box Protein O3, autoimmunity, Granulocyte-Macrophage Colony-Stimulating Factor, Cell Differentiation, GM-CSF, Th1 Cells, T-Cell, Stem Cell Research, HEK293 Cells, Antigen, Female, Stem Cell Research - Nonembryonic - Non-Human, T-Box Domain Proteins, pathogenic Th1, Autoimmune, Interleukin-1
الوصف: The transcription factor Foxo3 plays a crucial role in myeloid cell function but its role in lymphoid cells remains poorly defined. Here, we have shown that Foxo3 expression was increased after Tcell receptor engagement and played a specific role in the polarization of CD4+ Tcells toward pathogenic T helper 1 (Th1) cells producing interferon-γ (IFN-γ) and granulocyte monocyte colony stimulating factor (GM-CSF). Consequently, Foxo3-deficient mice exhibited reduced susceptibility to experimental autoimmune encephalomyelitis. At the molecular level, we identified Eomes as a direct target gene for Foxo3 in CD4+ Tcells and we have shown that lentiviral-based overexpression of Eomes in Foxo3-deficient CD4+ Tcells restored both IFN-γ and GM-CSF production.Thus, the Foxo3-Eomes pathway is central to achieve the complete specialized gene program required for pathogenic Th1 cell differentiation and development of neuroinflammation.
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=od_______325::32f7ac3f9600476185594d1329fa8741Test
https://escholarship.org/uc/item/7f71d7f8Test
حقوق: OPEN
رقم الانضمام: edsair.od.......325..32f7ac3f9600476185594d1329fa8741
قاعدة البيانات: OpenAIRE
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