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

PLoS One. 2014 Jul 15;9(7):e102331. doi: 10.1371/journal.pone.0102331. eCollection 2014.

Abstract

The effects of interferon-beta (IFN-β), one of the key immunotherapies used in multiple sclerosis (MS), on peripheral blood leukocytes and T cells have been extensively studied. B cells are a less abundant leukocyte type, and accordingly less is known about the B cell-specific response to IFN-β. To identify gene expression changes and pathways induced by IFN-β in B cells, we studied the in vitro response of human Epstein Barr-transformed B cells (lymphoblast cell lines-LCLs), and validated our results in primary B cells. 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 previously unrecognized as 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. Novel response genes identified herein, NEXN, DDX60L, IGFBP4, and HAPLN3, B cell receptor pathway genes, CD79B and SYK, and lymphocyte activation genes, LAG3 and IL27RA, were validated as IFN-β response genes in primary B cells. In this study new IFN-β response genes were identified in B cells, with possible implications to B cell-specific functions. The study's results emphasize the applicability of LCLs for studies of human B cell drug response. The usage of LCLs from patient-based repositories may facilitate future studies of drug response in MS and other immune-mediated disorders with a B cell component.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • B-Lymphocytes / metabolism*
  • Cell Line, Transformed
  • Gene Expression Profiling*
  • Herpesvirus 4, Human / physiology*
  • Humans
  • Interferon-beta / therapeutic use*
  • Lymphocyte Subsets
  • Multiple Sclerosis / drug therapy*
  • Multiple Sclerosis / genetics*

Substances

  • Interferon-beta

Associated data

  • GEO/GSE58240

Grants and funding

This work was supported by the National Multiple Sclerosis Society of the United States of America (RG 3520A1/1 to AM); and the Wolfson Family Charitable Trust, the Sacta-Rashi Foundation, the Technion's Vice-President for Research funds, the E. & S. Kronovet Fund for Medical Research, the American Technion Society, and the Association Technion France (to AM). RK was a recipient of the following fellowships: Israeli Ministry of Science and Technology fellowship for Arabs, Druze and Cherkessians, Gerald and Una Yakatan Fellowship, and Sondra and Robert Berk Fellowship. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.