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Deregulated microRNAs in CD4(+) T cells from individuals with latent tuberculosis versus active tuberculosis

The mechanisms of latent tuberculosis (TB) infection remain elusive. Roles of microRNA (miRNA) have been highlighted in pathogen–host interactions recently. To identify miRNAs involved in the immune response to TB, expression profiles of miRNAs in CD4(+) T cells from patients with latent TB, active...

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Autores principales: Fu, Yurong, Yi, Zhengjun, Li, Jianhua, Li, Ruifang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley & Sons Ltd 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3955156/
https://www.ncbi.nlm.nih.gov/pubmed/24373112
http://dx.doi.org/10.1111/jcmm.12205
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author Fu, Yurong
Yi, Zhengjun
Li, Jianhua
Li, Ruifang
author_facet Fu, Yurong
Yi, Zhengjun
Li, Jianhua
Li, Ruifang
author_sort Fu, Yurong
collection PubMed
description The mechanisms of latent tuberculosis (TB) infection remain elusive. Roles of microRNA (miRNA) have been highlighted in pathogen–host interactions recently. To identify miRNAs involved in the immune response to TB, expression profiles of miRNAs in CD4(+) T cells from patients with latent TB, active TB and healthy controls were investigated by microarray assay and validated by RT-qPCR. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were used to analyse the significant functions and involvement in signalling pathways of the differentially expressed miRNAs. To identify potential target genes for miR-29, interferon-γ (IFN-γ) mRNA expression was measured by RT-qPCR. Our results showed that 27 miRNAs were deregulated among the three groups. RT-qPCR results were generally consistent with the microarray data. We observed an inverse correlation between miR-29 level and IFN-γ mRNA expression in CD4(+) T cells. GO and KEGG pathway analysis showed that the possible target genes of deregulated miRNAs were significantly enriched in mitogen-activated protein kinase signalling pathway, focal adhesion and extracellular matrix receptor interaction, which might be involved in the transition from latent to active TB. In all, for the first time, our study revealed that some miRNAs in CD4(+) T cells were altered in latent and active TB. Function and pathway analysis highlighted the possible involvement of miRNA-deregulated mRNAs in TB. The study might help to improve understanding of the relationship between miRNAs in CD4(+) T cells and TB, and laid an important foundation for further identification of the underlying mechanisms of latent TB infection and its reactivation.
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spelling pubmed-39551562014-12-03 Deregulated microRNAs in CD4(+) T cells from individuals with latent tuberculosis versus active tuberculosis Fu, Yurong Yi, Zhengjun Li, Jianhua Li, Ruifang J Cell Mol Med Original Articles The mechanisms of latent tuberculosis (TB) infection remain elusive. Roles of microRNA (miRNA) have been highlighted in pathogen–host interactions recently. To identify miRNAs involved in the immune response to TB, expression profiles of miRNAs in CD4(+) T cells from patients with latent TB, active TB and healthy controls were investigated by microarray assay and validated by RT-qPCR. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were used to analyse the significant functions and involvement in signalling pathways of the differentially expressed miRNAs. To identify potential target genes for miR-29, interferon-γ (IFN-γ) mRNA expression was measured by RT-qPCR. Our results showed that 27 miRNAs were deregulated among the three groups. RT-qPCR results were generally consistent with the microarray data. We observed an inverse correlation between miR-29 level and IFN-γ mRNA expression in CD4(+) T cells. GO and KEGG pathway analysis showed that the possible target genes of deregulated miRNAs were significantly enriched in mitogen-activated protein kinase signalling pathway, focal adhesion and extracellular matrix receptor interaction, which might be involved in the transition from latent to active TB. In all, for the first time, our study revealed that some miRNAs in CD4(+) T cells were altered in latent and active TB. Function and pathway analysis highlighted the possible involvement of miRNA-deregulated mRNAs in TB. The study might help to improve understanding of the relationship between miRNAs in CD4(+) T cells and TB, and laid an important foundation for further identification of the underlying mechanisms of latent TB infection and its reactivation. John Wiley & Sons Ltd 2014-03 2013-12-25 /pmc/articles/PMC3955156/ /pubmed/24373112 http://dx.doi.org/10.1111/jcmm.12205 Text en © 2013 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine. http://creativecommons.org/licenses/by/3.0/ This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Articles
Fu, Yurong
Yi, Zhengjun
Li, Jianhua
Li, Ruifang
Deregulated microRNAs in CD4(+) T cells from individuals with latent tuberculosis versus active tuberculosis
title Deregulated microRNAs in CD4(+) T cells from individuals with latent tuberculosis versus active tuberculosis
title_full Deregulated microRNAs in CD4(+) T cells from individuals with latent tuberculosis versus active tuberculosis
title_fullStr Deregulated microRNAs in CD4(+) T cells from individuals with latent tuberculosis versus active tuberculosis
title_full_unstemmed Deregulated microRNAs in CD4(+) T cells from individuals with latent tuberculosis versus active tuberculosis
title_short Deregulated microRNAs in CD4(+) T cells from individuals with latent tuberculosis versus active tuberculosis
title_sort deregulated micrornas in cd4(+) t cells from individuals with latent tuberculosis versus active tuberculosis
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3955156/
https://www.ncbi.nlm.nih.gov/pubmed/24373112
http://dx.doi.org/10.1111/jcmm.12205
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