Form of presentation | Articles in international journals and collections |
Year of publication | 2017 |
Язык | английский |
|
Kotov Nikolay Viktorovich, author
Salakhieva Diana Vitalevna, author
|
|
I. I Sadreev , Michael Z, Q Chen , Yoshinori Umezawa , Claudia Kemper, Gavin I Welsh Ildar I, author
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Bibliographic description in the original language |
Ildar I Sadreev, The competitive nature of STAT complex formation drives phenotype switching of T cells /Ildar I Sadreev, Michael Z Q Chen, Yoshinori Umezawa, Vadim N Biktashev, Claudia Kemper, Diana V Salakhieva, Gavin I Welsh, Nikolay V Kotov.-2017.-Cite as: arXiv:1701.05503 [q-bio.MN] |
Annotation |
Signal 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 |
Keywords |
Quantitative Biology, Molecular Networks |
The name of the journal |
IMMUNOLOGY
|
URL |
https://arxiv.org/abs/1701.05503 |
Please use this ID to quote from or refer to the card |
https://repository.kpfu.ru/eng/?p_id=170473&p_lang=2 |
Full metadata record |
Field DC |
Value |
Language |
dc.contributor.author |
Kotov Nikolay Viktorovich |
ru_RU |
dc.contributor.author |
Salakhieva Diana Vitalevna |
ru_RU |
dc.contributor.author |
I. I Sadreev , Michael Z, Q Chen , Yoshinori Umezawa , Claudia Kemper, Gavin I Welsh Ildar I |
ru_RU |
dc.date.accessioned |
2017-01-01T00:00:00Z |
ru_RU |
dc.date.available |
2017-01-01T00:00:00Z |
ru_RU |
dc.date.issued |
2017 |
ru_RU |
dc.identifier.citation |
Ildar I Sadreev, The competitive nature of STAT complex formation drives phenotype switching of T cells /Ildar I Sadreev, Michael Z Q Chen, Yoshinori Umezawa, Vadim N Biktashev, Claudia Kemper, Diana V Salakhieva, Gavin I Welsh, Nikolay V Kotov.-2017.-Cite as: arXiv:1701.05503 [q-bio.MN] |
ru_RU |
dc.identifier.uri |
https://repository.kpfu.ru/eng/?p_id=170473&p_lang=2 |
ru_RU |
dc.description.abstract |
IMMUNOLOGY |
ru_RU |
dc.description.abstract |
Signal 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 |
ru_RU |
dc.language.iso |
ru |
ru_RU |
dc.subject |
Quantitative Biology |
ru_RU |
dc.subject |
Molecular Networks |
ru_RU |
dc.title |
The competitive nature of STAT complex formation drives phenotype switching of T cells |
ru_RU |
dc.type |
Articles in international journals and collections |
ru_RU |
|