INTERFEROME v2.0: an updated database of annotated interferon-regulated genes

Abstract

Interferome v2.0 (http://interferome.its.monash.edu.au/interferome/) is an update of an earlier version of the Interferome DB published in the 2009 NAR database edition. Vastly improved computational infrastructure now enables more complex and faster queries, and supports more data sets from types I, II and III interferon (IFN)-treated cells, mice or humans. Quantitative, MIAME compliant data are collected, subjected to thorough, standardized, quantitative and statistical analyses and then significant changes in gene expression are uploaded. Comprehensive manual collection of metadata in v2.0 allows flexible, detailed search capacity including the parameters: range of -fold change, IFN type, concentration and time, and cell/tissue type. There is no limit to the number of genes that can be used to search the database in a single query. Secondary analysis such as gene ontology, regulatory factors, chromosomal location or tissue expression plots of IFN-regulated genes (IRGs) can be performed in Interferome v2.0, or data can be downloaded in convenient text formats compatible with common secondary analysis programs. Given the importance of IFN to innate immune responses in infectious, inflammatory diseases and cancer, this upgrade of the Interferome to version 2.0 will facilitate the identification of gene signatures of importance in the pathogenesis of these diseases.

Anti-GITR Agonist Therapy Intrinsically Enhances CD8 T Cell Responses to Chronic Lymphocytic Choriomeningitis Virus (LCMV), Thereby Circumventing LCMV-Induced Downregulation of Costimulatory GITR Ligand on APC

“…5F, 5G and data not shown). The total number of IFN-g/CD107a coproducers following ex vivo GP [33][34][35][36][37][38][39][40][41] peptide restimulation was consistently, but not significantly higher, in DTA-1-treated animals (Fig. 5F).…”

“…Splenocytes were stained with tetramer and surface stain Abs for 1 h at 4˚C, after which cells were washed thoroughly and fixed in 4% paraformaldehyde for 30 min at 4˚C. For intracellular cytokine staining, splenocytes were cultured in complete medium with brefeldin A and monensin (BD Biosciences; catalog 554715) with 1 mg/ml H-2D b -restricted LCMV NP 396-404 , GP [33][34][35][36][37][38][39][40][41] , or GP 276-286 (Anaspec, Fremont, CA) and 0.5 mg/ml anti-CD107a or IgG1 isotype control (BD Biosciences) for 5 h, or 4 mg/ml I-A b -restricted LCMV GP 61-80 with 20 U/ml murine rIL-2 (eBioscience) for 5 h. Cells were then surface stained, fixed, permeabilized (BD Biosciences), and stained for intracellular cytokine production.…”

“…Freshly isolated splenocytes were incubated with or without 1 mM LCMV GP [33][34][35][36][37][38][39][40][41] peptide (Anaspec) for 1 h in complete medium at 37˚C. Cells were then washed thoroughly and labeled with 1 mM (unpulsed targets) or 10 mM (GP 33-41 pulsed targets) CFSE for 10 min at 37˚C in 0.1% BSA in PBS solution.…”

C-type lectin receptor DCIR modulates immunity to tuberculosis by sustaining type I interferon signaling in dendritic cells

“…S2 A and B), we first evaluated the impact of this CLR in a global and unbiased manner through genomewide transcriptome analysis of bone marrow-derived DCs from WT and DCIR-KO animals before and during M. tuberculosis infection. Functional gene set enrichment analysis (GSEA) and interrogation of the Interferome database (21) revealed that a significant fraction of genes, which were down-regulated in DCIR-KO DCs compared with WT cells, was dependent on type I IFN and/or included genes involved in defense to viruses (SI Appendix, Fig. S3 and Fig.…”

Interfering with Immunity: Detrimental Role of Type I IFNs during Infection

“…Bioinformatic approaches have led to the identification of IFN-inducible gene signatures (38)(39)(40), although the precise function of individual IRGs in an immune response is still being elucidated (39). This IFN gene signature is traditionally referred to as the "antiviral state" (41) (45).…”