Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

SLE serum induced transcripts regulated by IFNa2b

ABSTRACT: To explore the full extent of IFN-regulated transcriptional changes, we exposed monocytes from two healthy donors to recombinant type I IFN (IFN-M-NM-12b) in vitro. RNA was extracted at 6 hrs and the expression data was normalized to that of monocytes cultured with medium. Blood monocytes isolated from healthy volunteers were incubated with 20% autologous serum alone or in the presence of 1000 U/ml of IFNM-NM-12b (Schering Plough, Kenilworth, NJ) in 6-well plates at a concentration of 106 monocytes per well in 3 ml of media. After incubation for six hours at 37 M-bM-^AM-0C, cells were harvested and RNA was extracted.

ORGANISM(S): Homo sapiens

SUBMITTER: Nicole Baldwin

PROVIDER: E-GEOD-46921 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

IFN priming is necessary but not sufficient to turn on a migratory dendritic cell program in lupus monocytes.

Rodriguez-Pla Alicia A Patel Pinakeen P Maecker Holden T HT Rossello-Urgell Jose J Baldwin Nicole N Bennett Lynda L Cantrell Victoria V Baisch Jeanine J Punaro Marilynn M Gotte Alisa A Nassi Lorien L Wright Tracey T Palucka Anna Karolina AK Banchereau Jacques J Pascual Virginia V

Journal of immunology (Baltimore, Md. : 1950) 20140514 12

Blood monocytes from children with systemic lupus erythematosus (SLE) behave similar to dendritic cells (DCs), and SLE serum induces healthy monocytes to differentiate into DCs in a type I IFN-dependent manner. In this study, we found that these monocytes display significant transcriptional changes, including a prominent IFN signature, compared with healthy controls. Few of those changes, however, explain DC function. Exposure to allogeneic T cells in vitro reprograms SLE monocytes to acquire DC ...[more]

PMID: 24829414

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Project description:The research hypothesis was that the unique expression profile of monocytes in response to Interferon-beta (IFN-Î²) might be masked by the response profile of the more abundant T cells. The analysis of monocytes response may highlight novel IFN-Î² functions and pathways that have not been recognized previously. The aim of this study was to characterized the IFN-Î² transcriptional response in monocytes, a small but influential cell-subset, using gene expression profile and pathway analysis. The expression profiles of purified human monocytes and T cells pulse with IFN-Î² overnight were compared, and revealed 276 and 42 Differentially Expressed Genes (DEGs) in monocytes and T cells respectively, with only 5 genes common to both sets. Many of the DEGs detected in monocytes were novel with respect to the recognized IFN-Î² response, and included genes involved in immune-specific activities, communication between cells, regulation of apoptosis, cell migration, and protein translation. Network and pathway analysis of the T cells response revealed the familiar immune pathways, response to virus pathways, and IFN canonical pathway. In monocytes, however, we detected along with known IFN-Î²-related pathways, such as cell migration also pathways that had not been previously described in the context of IFN-Î² response, such as the High-Mobility Group Box-1 (HMGB1) signaling pathway. However, most DEGs in monocytes did not cluster to specific networks or canonical pathways. The monocyte-specific DEGs and pathways described herein are beyond the current knowledge regarding the biology of the IFN-Î² response and the differential response to IFN-Î² of monocytes versus T cells described emphasizes the importance of cell-specific studies for elucidating the spectrum of cytokine-mediated immunomodulation. Monocytes and T lymphocytes were isolated from 3 healthy volunteers. For each sample the expression profile of untreated cells was compared to the profile of IFN-Î² treated cells, i.e. 4 samples from each donor (2 cell types, with and without treatment), 12 samples total.

Dataset Information

SLE serum induced transcripts regulated by IFNa2b

Publications

IFN priming is necessary but not sufficient to turn on a migratory dendritic cell program in lupus monocytes.

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