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An atlas of mouse CD4(+) T cell transcriptomes
BACKGROUND: CD4(+) T cells are key regulators of the adaptive immune system and can be divided into T helper (Th) cells and regulatory T (Treg) cells. During an immune response Th cells mature from a naive state into one of several effector subtypes that exhibit distinct functions. The transcription...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4384382/ https://www.ncbi.nlm.nih.gov/pubmed/25886751 http://dx.doi.org/10.1186/s13062-015-0045-x |
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author | Stubbington, Michael JT Mahata, Bidesh Svensson, Valentine Deonarine, Andrew Nissen, Jesper K Betz, Alexander G Teichmann, Sarah A |
author_facet | Stubbington, Michael JT Mahata, Bidesh Svensson, Valentine Deonarine, Andrew Nissen, Jesper K Betz, Alexander G Teichmann, Sarah A |
author_sort | Stubbington, Michael JT |
collection | PubMed |
description | BACKGROUND: CD4(+) T cells are key regulators of the adaptive immune system and can be divided into T helper (Th) cells and regulatory T (Treg) cells. During an immune response Th cells mature from a naive state into one of several effector subtypes that exhibit distinct functions. The transcriptional mechanisms that underlie the specific functional identity of CD4(+) T cells are not fully understood. RESULTS: To assist investigations into the transcriptional identity and regulatory processes of these cells we performed mRNA-sequencing on three murine T helper subtypes (Th1, Th2 and Th17) as well as on splenic Treg cells and induced Treg (iTreg) cells. Our integrated analysis of this dataset revealed the gene expression changes associated with these related but distinct cellular identities. Each cell subtype differentially expresses a wealth of ‘subtype upregulated’ genes, some of which are well known whilst others promise new insights into signalling processes and transcriptional regulation. We show that hundreds of genes are regulated purely by alternative splicing to extend our knowledge of the role of post-transcriptional regulation in cell differentiation. CONCLUSIONS: This CD4(+) transcriptome atlas provides a valuable resource for the study of CD4(+) T cell populations. To facilitate its use by others, we have made the data available in an easily accessible online resource at www.th-express.org. REVIEWERS: This article was reviewed by Wayne Hancock, Christine Wells and Erik van Nimwegen. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s13062-015-0045-x) contains supplementary material, which is available to authorized users. |
format | Online Article Text |
id | pubmed-4384382 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-43843822015-04-04 An atlas of mouse CD4(+) T cell transcriptomes Stubbington, Michael JT Mahata, Bidesh Svensson, Valentine Deonarine, Andrew Nissen, Jesper K Betz, Alexander G Teichmann, Sarah A Biol Direct Research BACKGROUND: CD4(+) T cells are key regulators of the adaptive immune system and can be divided into T helper (Th) cells and regulatory T (Treg) cells. During an immune response Th cells mature from a naive state into one of several effector subtypes that exhibit distinct functions. The transcriptional mechanisms that underlie the specific functional identity of CD4(+) T cells are not fully understood. RESULTS: To assist investigations into the transcriptional identity and regulatory processes of these cells we performed mRNA-sequencing on three murine T helper subtypes (Th1, Th2 and Th17) as well as on splenic Treg cells and induced Treg (iTreg) cells. Our integrated analysis of this dataset revealed the gene expression changes associated with these related but distinct cellular identities. Each cell subtype differentially expresses a wealth of ‘subtype upregulated’ genes, some of which are well known whilst others promise new insights into signalling processes and transcriptional regulation. We show that hundreds of genes are regulated purely by alternative splicing to extend our knowledge of the role of post-transcriptional regulation in cell differentiation. CONCLUSIONS: This CD4(+) transcriptome atlas provides a valuable resource for the study of CD4(+) T cell populations. To facilitate its use by others, we have made the data available in an easily accessible online resource at www.th-express.org. REVIEWERS: This article was reviewed by Wayne Hancock, Christine Wells and Erik van Nimwegen. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s13062-015-0045-x) contains supplementary material, which is available to authorized users. BioMed Central 2015-04-03 /pmc/articles/PMC4384382/ /pubmed/25886751 http://dx.doi.org/10.1186/s13062-015-0045-x Text en © Stubbington et al.; licensee BioMed Central. 2015 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Research Stubbington, Michael JT Mahata, Bidesh Svensson, Valentine Deonarine, Andrew Nissen, Jesper K Betz, Alexander G Teichmann, Sarah A An atlas of mouse CD4(+) T cell transcriptomes |
title | An atlas of mouse CD4(+) T cell transcriptomes |
title_full | An atlas of mouse CD4(+) T cell transcriptomes |
title_fullStr | An atlas of mouse CD4(+) T cell transcriptomes |
title_full_unstemmed | An atlas of mouse CD4(+) T cell transcriptomes |
title_short | An atlas of mouse CD4(+) T cell transcriptomes |
title_sort | atlas of mouse cd4(+) t cell transcriptomes |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4384382/ https://www.ncbi.nlm.nih.gov/pubmed/25886751 http://dx.doi.org/10.1186/s13062-015-0045-x |
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