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dc.contributor.authorSadreev, II
dc.contributor.authorChen, MZQ
dc.contributor.authorUmezawa, Y
dc.contributor.authorBiktashev, VN
dc.contributor.authorKemper, C
dc.contributor.authorSalakhieva, DV
dc.contributor.authorWelsh, GI
dc.contributor.authorKotov, NV
dc.date.accessioned2017-02-14T09:49:38Z
dc.date.issued2017
dc.description.abstractSignal transducers and activators of transcription (STATs) are key molecular determinants of T cell fate and effector function. A number of inflammatory diseases are characterized by an altered balance of T cell phenotypes and cytokine secretion. STATs, therefore, represent viable therapeutic targets in numerous pathologies. However, the underlying mechanisms of how the same STAT proteins regulate both the development of different T cell phenotypes and their plasticity during changes in extracellular conditions remain unclear. In this study, we investigated the STAT mediated regulation of T cell phenotype formation and plasticity using mathematical modeling and experimental data for intracellular STAT signaling proteins. The close fit of our model predictions to the experimental data for IFN-{\gamma} to IL-10 switching allows us to propose a potential mechanism for T cell switching that regulates human Th1/Tr1 responses. According to this mechanism, T cell phenotype switching is due to the relative redistribution of STAT dimer complexes caused by the extracellular cytokine-dependent STAT competition effects. The proposed model is applicable to a number of STAT signaling circuits.en_GB
dc.identifier.citationarXiv:1701.05503v1 [q-bio.MN]en_GB
dc.identifier.urihttp://hdl.handle.net/10871/25826
dc.language.isoenen_GB
dc.publisherarXiv.orgen_GB
dc.relation.urlhttp://arxiv.org/abs/1701.05503v1en_GB
dc.subjectq-bio.MNen_GB
dc.titleThe competitive nature of STAT complex formation drives phenotype switching of T cellsen_GB
dc.typeArticleen_GB
dc.date.available2017-02-14T09:49:38Z
dc.descriptionThis is the author accepted manuscript.en_GB
dc.identifier.journalArXiven_GB


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