Dataset Information


Corral2021 - Interplay between SMAD2 and STAT5A regulating IL-17A/F expression in Th cells.

ABSTRACT: IL-17A and F are critical cytokines in anti-microbial immunity but also contribute to auto-immune pathologies. Recent evidence suggests that they may be differentially produced by T-helper (Th) cells but the underlying mechanisms remain unknown. To address this question, a logical model containing 82 components and 136 regulatory links was developed and calibrated with original flow cytometry data using naive CD4+ T cells in conditions inducing either IL-17A or F. Model analyses led to the identification of the transcription factors NFAT2A, STAT5A and Smad2 as key components explaining the differential expression of IL-17A and IL-17F, with STAT5A controlling IL-17F expression, and an interplay of NFAT2A, STAT5A and Smad2 controlling IL-17A expression.

SUBMITTER: Denis Thieffry  

PROVIDER: MODEL2101150001 | BioModels | 2021-04-06


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MODEL2101150001?filename=Corral_ThIL17diff_15jan2021.sbml Other
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T-bet and eomesodermin play critical roles in directing T cell differentiation to Th1 versus Th17.

Yang Yu Y   Xu Jiangnan J   Niu Yanyan Y   Bromberg Jonathan S JS   Ding Yaozhong Y  

Journal of immunology (Baltimore, Md. : 1950) 20081201 12

Th1 and Th17 cells are crucial in immune regulation and autoimmune disease development. By adding Stat6 deficiency to T-bet deficiency, and thus negating effects from elevated levels of IL-4/Stat6/GATA3 Th2 signals in T-bet-deficient cells, we investigated the signals important for Th1 and Th17 cell differentiation and their role in colitis development. The data reveal that Eomesodermin compensates T-bet deficiency for IFN-gamma and Th1 development. However, without T-bet, IFN-gamma production a  ...[more]

Publication: 1/86

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