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Deregulated micro RNA s in CD 4 + T cells from individuals with latent tuberculosis versus active tuberculosis
Author(s) -
Fu Yurong,
Yi Zhengjun,
Li Jianhua,
Li Ruifang
Publication year - 2014
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.12205
Subject(s) - kegg , microrna , biology , microarray , microarray analysis techniques , gene , gene expression , latent tuberculosis , signal transduction , mycobacterium tuberculosis , gene expression profiling , microbiology and biotechnology , genetics , tuberculosis , transcriptome , medicine , pathology
The mechanisms of latent tuberculosis ( TB ) infection remain elusive. Roles of micro RNA (mi RNA ) have been highlighted in pathogen–host interactions recently. To identify mi RNA s involved in the immune response to TB , expression profiles of mi RNA s in CD 4 + 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 mi RNA s. To identify potential target genes for miR‐29, interferon‐γ ( IFN ‐γ) m RNA expression was measured by RT ‐q PCR . Our results showed that 27 mi RNA s were deregulated among the three groups. RT ‐q PCR results were generally consistent with the microarray data. We observed an inverse correlation between miR‐29 level and IFN ‐γ m RNA expression in CD 4 + T cells. GO and KEGG pathway analysis showed that the possible target genes of deregulated mi RNA s 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 mi RNA s in CD 4 + T cells were altered in latent and active TB . Function and pathway analysis highlighted the possible involvement of mi RNA ‐deregulated m RNA s in TB . The study might help to improve understanding of the relationship between mi RNA s in CD 4 + 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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