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Gene expression profiling of the response to interferon beta in EBV-transformed and primary B cells of patients with multiple sclerosis

ABSTRACT: To identify gene expression changes and pathways induced by interferon-β (IFN-β) in B cells, we studied the in vitro response of EBV-transformed B cells (lymphoblast cell lines-LCLs). LCLs were derived from an MS patient repository. Whole genome expression analysis identified 115 genes that were more than two-fold differentially up-regulated following IFN-β exposure, with over 50 novel IFN-β response genes. Pathways analysis demonstrated that IFN-β affected LCLs in a similar manner to other cell types by activating known IFN-β canonical pathways. Additionally, IFN-β increased the expression of innate immune response genes, while down-regulating many B cell receptor pathway genes and genes involved in adaptive immune responses. Several of the novel response genes were tested and validated as IFN-β response genes in human primary B cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE58240 | GEO | 2014/07/30

SECONDARY ACCESSION(S): PRJNA251683

REPOSITORIES: GEO

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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.

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Gene expression profiling of the response to interferon beta in EBV-transformed and primary B cells of patients with multiple sclerosis

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