Please use this identifier to cite or link to this item: https://hdl.handle.net/10356/80635
Title: Continuous time Bayesian networks identify Prdm1 as a negative regulator of TH17 cell differentiation in humans
Authors: Acerbi, Enzo
Viganò, Elena
Poidinger, Michael
Mortellaro, Alessandra
Zelante, Teresa
Stella, Fabio
Keywords: PRDM1 Protein, Human
Cell Differentiation
DRNTU::Science::Biological sciences
Issue Date: 2016
Source: Acerbi, E., Viganò, E., Poidinger, M., Mortellaro, A., Zelante, T., & Stella, F. (2016). Continuous time Bayesian networks identify Prdm1 as a negative regulator of TH17 cell differentiation in humans. Scientific Reports, 6, 23128-. doi:10.1038/srep23128
Series/Report no.: Scientific Reports
Abstract: T helper 17 (TH17) cells represent a pivotal adaptive cell subset involved in multiple immune disorders in mammalian species. Deciphering the molecular interactions regulating TH17 cell differentiation is particularly critical for novel drug target discovery designed to control maladaptive inflammatory conditions. Using continuous time Bayesian networks over a time-course gene expression dataset, we inferred the global regulatory network controlling TH17 differentiation. From the network, we identified the Prdm1 gene encoding the B lymphocyte-induced maturation protein 1 as a crucial negative regulator of human TH17 cell differentiation. The results have been validated by perturbing Prdm1 expression on freshly isolated CD4+ naïve T cells: reduction of Prdm1 expression leads to augmentation of IL-17 release. These data unravel a possible novel target to control TH17 polarization in inflammatory disorders. Furthermore, this study represents the first in vitro validation of continuous time Bayesian networks as gene network reconstruction method and as hypothesis generation tool for wet-lab biological experiments.
URI: https://hdl.handle.net/10356/80635
http://hdl.handle.net/10220/46573
DOI: 10.1038/srep23128
Rights: © 2016 The Authors (Nature Publishing Group). This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
Fulltext Permission: open
Fulltext Availability: With Fulltext
Appears in Collections:SCELSE Journal Articles

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