Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Characterization of microRNA Expression Profiles in human primary differentiated T lymphocytes

ABSTRACT: Activation of the T cell-mediated immune response has been associated with changes in the expression of specific miRNAs. However, the role of miRNAs in the development of an effective immune response is just beginning to be explored. Here we report a microRNA expression profile showing a list of microRNAs, which are highly up-regulated or down-regulated in human memory T cells compared to naive T cells, thus suggesting a possible role of these microRNAs in T lymphocyte differentiation. Keywords: Primary Tissue miRNA Expression profile We used microarrays to profile miRNA expression in human naive and central memory CD4+ and CD8+ T lymphocytes

ORGANISM(S): Homo sapiens

SUBMITTER: Graziella Curtale

PROVIDER: E-GEOD-16453 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

An emerging player in the adaptive immune response: microRNA-146a is a modulator of IL-2 expression and activation-induced cell death in T lymphocytes.

Curtale Graziella G Citarella Franca F Carissimi Claudia C Goldoni Marina M Carucci Nicoletta N Fulci Valerio V Franceschini Debora D Meloni Francesca F Barnaba Vincenzo V Macino Giuseppe G

Blood 20091112 2

Activation of the T cell-mediated immune response has been associated with changes in the expression of specific microRNAs (miRNAs). However, the role of miRNAs in the development of an effective immune response is just beginning to be explored. This study focuses on the functional role of miR-146a in T lymphocyte-mediated immune response and provides interesting clues on the transcriptional regulation of miR-146a during T-cell activation. We show that miR-146a is low in human naive T cells and ...[more]

PMID: 19965651

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Project description:MicroRNAs (miRNAs) in body fluids are candidate diagnostics for a variety of conditions and diseases, including breast cancer. One premise for using extracellular miRNAs to diagnose disease is the notion that the abundance of the miRNAs in body fluids reflects their abundance in the abnormal cells causing the disease. As a result, the search for such diagnostics in body fluids has focused on miRNAs that are abundant in the cells of origin. Here we report that released miRNAs do not necessarily reflect the abundance of miRNA in the cell of origin. We find that release of miRNAs from cells into blood, milk and ductal fluids is selective and that the selection of released miRNAs may correlate with malignancy. In particular, the bulk of miR-451 and miR-1246 produced by malignant mammary epithelial cells was released, but the majority of these miRNAs produced by non-malignant mammary epithelial cells was retained. Our findings suggest the existence of a cellular selection mechanism for miRNA release and indicate that the extracellular and cellular miRNA profiles differ. This selective release of miRNAs is an important consideration for the identification of circulating miRNAs as biomarkers of disease. miRNA microarrays were screened by LC Sciences. One microgram of MCF7 cellular RNA preparation was labeled with Cy3, and one microgram of the extracellular RNA samples was labeled with Cy5. In brief, the RNA was labeled with Cy5 or Cy3 and hybridized to LCSciences standard arrays for mature miRNA of all species available in the Sanger miRBase database (Release 12.0). The data were analyzed including background subtraction, using a LOWESS (locally weighted regression) method on the background-subtracted data. Only transcripts with a signal intensity higher than 3X (background SD) and spot CV<0.5. CV was calculated by (SD)/(signal intensity), and in which repeating probes on the array produced signals from at least 50% of the repeating probes are above detection level.

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Dataset Information

Characterization of microRNA Expression Profiles in human primary differentiated T lymphocytes

Publications

An emerging player in the adaptive immune response: microRNA-146a is a modulator of IL-2 expression and activation-induced cell death in T lymphocytes.

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