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No differential gene expression for CD4(+) T cells of MS patients and healthy controls

BACKGROUND: Multiple sclerosis-associated genetic variants indicate that the adaptive immune system plays an important role in the risk of developing multiple sclerosis. It is currently not well understood how these multiple sclerosis-associated genetic variants contribute to multiple sclerosis risk...

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Autores principales: Brorson, Ina S, Eriksson, Anna, Leikfoss, Ingvild S, Celius, Elisabeth G, Berg-Hansen, Pål, Barcellos, Lisa F, Berge, Tone, Harbo, Hanne F, Bos, Steffan D
Formato: Online Artículo Texto
Lenguaje:English
Publicado: SAGE Publications 2019
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Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6566490/
https://www.ncbi.nlm.nih.gov/pubmed/31223483
http://dx.doi.org/10.1177/2055217319856903
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author Brorson, Ina S
Eriksson, Anna
Leikfoss, Ingvild S
Celius, Elisabeth G
Berg-Hansen, Pål
Barcellos, Lisa F
Berge, Tone
Harbo, Hanne F
Bos, Steffan D
author_facet Brorson, Ina S
Eriksson, Anna
Leikfoss, Ingvild S
Celius, Elisabeth G
Berg-Hansen, Pål
Barcellos, Lisa F
Berge, Tone
Harbo, Hanne F
Bos, Steffan D
author_sort Brorson, Ina S
collection PubMed
description BACKGROUND: Multiple sclerosis-associated genetic variants indicate that the adaptive immune system plays an important role in the risk of developing multiple sclerosis. It is currently not well understood how these multiple sclerosis-associated genetic variants contribute to multiple sclerosis risk. CD4(+) T cells are suggested to be involved in multiple sclerosis disease processes. OBJECTIVE: We aim to identify CD4(+) T cell differential gene expression between multiple sclerosis patients and healthy controls in order to understand better the role of these cells in multiple sclerosis. METHODS: We applied RNA sequencing on CD4(+) T cells from multiple sclerosis patients and healthy controls. RESULTS: We did not identify significantly differentially expressed genes in CD4(+) T cells from multiple sclerosis patients. Furthermore, pathway analyses did not identify enrichment for specific pathways in multiple sclerosis. When we investigated genes near multiple sclerosis-associated genetic variants, we did not observe significant enrichment of differentially expressed genes. CONCLUSION: We conclude that CD4(+) T cells from multiple sclerosis patients do not show significant differential gene expression. Therefore, gene expression studies of all circulating CD4(+) T cells may not result in viable biomarkers. Gene expression studies of more specific subsets of CD4(+) T cells remain justified to understand better which CD4(+) T cell subsets contribute to multiple sclerosis pathology.
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spelling pubmed-65664902019-06-20 No differential gene expression for CD4(+) T cells of MS patients and healthy controls Brorson, Ina S Eriksson, Anna Leikfoss, Ingvild S Celius, Elisabeth G Berg-Hansen, Pål Barcellos, Lisa F Berge, Tone Harbo, Hanne F Bos, Steffan D Mult Scler J Exp Transl Clin Original Research Paper BACKGROUND: Multiple sclerosis-associated genetic variants indicate that the adaptive immune system plays an important role in the risk of developing multiple sclerosis. It is currently not well understood how these multiple sclerosis-associated genetic variants contribute to multiple sclerosis risk. CD4(+) T cells are suggested to be involved in multiple sclerosis disease processes. OBJECTIVE: We aim to identify CD4(+) T cell differential gene expression between multiple sclerosis patients and healthy controls in order to understand better the role of these cells in multiple sclerosis. METHODS: We applied RNA sequencing on CD4(+) T cells from multiple sclerosis patients and healthy controls. RESULTS: We did not identify significantly differentially expressed genes in CD4(+) T cells from multiple sclerosis patients. Furthermore, pathway analyses did not identify enrichment for specific pathways in multiple sclerosis. When we investigated genes near multiple sclerosis-associated genetic variants, we did not observe significant enrichment of differentially expressed genes. CONCLUSION: We conclude that CD4(+) T cells from multiple sclerosis patients do not show significant differential gene expression. Therefore, gene expression studies of all circulating CD4(+) T cells may not result in viable biomarkers. Gene expression studies of more specific subsets of CD4(+) T cells remain justified to understand better which CD4(+) T cell subsets contribute to multiple sclerosis pathology. SAGE Publications 2019-06-13 /pmc/articles/PMC6566490/ /pubmed/31223483 http://dx.doi.org/10.1177/2055217319856903 Text en © The Author(s) 2019 http://creativecommons.org/licenses/by-nc/4.0/ Creative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).
spellingShingle Original Research Paper
Brorson, Ina S
Eriksson, Anna
Leikfoss, Ingvild S
Celius, Elisabeth G
Berg-Hansen, Pål
Barcellos, Lisa F
Berge, Tone
Harbo, Hanne F
Bos, Steffan D
No differential gene expression for CD4(+) T cells of MS patients and healthy controls
title No differential gene expression for CD4(+) T cells of MS patients and healthy controls
title_full No differential gene expression for CD4(+) T cells of MS patients and healthy controls
title_fullStr No differential gene expression for CD4(+) T cells of MS patients and healthy controls
title_full_unstemmed No differential gene expression for CD4(+) T cells of MS patients and healthy controls
title_short No differential gene expression for CD4(+) T cells of MS patients and healthy controls
title_sort no differential gene expression for cd4(+) t cells of ms patients and healthy controls
topic Original Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6566490/
https://www.ncbi.nlm.nih.gov/pubmed/31223483
http://dx.doi.org/10.1177/2055217319856903
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