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      Late multiple organ surge in interferon-regulated target genes characterizes staphylococcal enterotoxin B lethality.

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          Abstract

          Bacterial superantigens are virulence factors that cause toxic shock syndrome. Here, the genome-wide, temporal response of mice to lethal intranasal staphylococcal enterotoxin B (SEB) challenge was investigated in six tissues.

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          RIG-I-mediated antiviral responses to single-stranded RNA bearing 5'-phosphates.

          Andreas Pichlmair, Oliver Schulz, Choon Ping Tan … (2006)
          Double-stranded RNA (dsRNA) produced during viral replication is believed to be the critical trigger for activation of antiviral immunity mediated by the RNA helicase enzymes retinoic acid-inducible gene I (RIG-I) and melanoma differentiation-associated gene 5 (MDA5). We showed that influenza A virus infection does not generate dsRNA and that RIG-I is activated by viral genomic single-stranded RNA (ssRNA) bearing 5'-phosphates. This is blocked by the influenza protein nonstructured protein 1 (NS1), which is found in a complex with RIG-I in infected cells. These results identify RIG-I as a ssRNA sensor and potential target of viral immune evasion and suggest that its ability to sense 5'-phosphorylated RNA evolved in the innate immune system as a means of discriminating between self and nonself.
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            INTERFEROME v2.0: an updated database of annotated interferon-regulated genes

            Irina Rusinova, Sam Forster, Simon Yu … (2012)
            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.
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              Recognition of cytosolic DNA activates an IRF3-dependent innate immune response.

              Daniel B Stetson, Ruslan Medzhitov (2006)
              Nucleic acid recognition upon viral infection triggers type I interferon production. Viral RNA is detected by both endosomal, TLR-dependent and cytosolic, RIG-I/MDA5-dependent pathways. TLR9 is the only known sensor of foreign DNA; it is unknown whether innate immune recognition of DNA exists in the cytosol. Here we present evidence that cytosolic DNA activates a potent type I interferon response to the invasive bacterium Listeria monocytogenes. The noninvasive Legionella pneumophila triggers an identical response through its type IV secretion system. Activation of type I interferons by cytosolic DNA is TLR independent and requires IRF3 but occurs without detectable activation of NF-kappaB and MAP kinases. Microarray analyses reveal a unique but overlapping gene-expression program activated by cytosolic DNA compared to TLR9- and RIG-I/MDA5-dependent responses. These findings define an innate immune response to DNA linked to type I interferon production.
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                Author and article information

                Journal
                Journal ID (iso-abbrev): PLoS ONE
                Title: PloS one
                Publisher: Public Library of Science (PLoS)
                ISSN (Electronic): 1932-6203
                ISSN (Print): 1932-6203
                Publication date (Electronic): 2014
                Volume: 9
                Issue: 2
                Affiliations
                [1 ] Functional Genomics and Proteomics Facility, Critical Care Medicine Department, Clinical Research Center, National Institutes of Health, Bethesda, Maryland, United States of America.
                [2 ] Mathematical and Statistical Computing Laboratory, Center for Information Technology, National Institutes of Health, Bethesda, Maryland, United States of America.
                [3 ] Division of Veterinary Resources, Office of Research Services, National Institutes of Health, Bethesda, Maryland, United States of America.
                [4 ] Integrated Toxicology Division, U.S. Army Medical Research Institute of Infectious Diseases, Fort Detrick, Maryland, United States of America.
                Article
                Publisher Item ID: PONE-D-13-27443
                DOI: 10.1371/journal.pone.0088756
                PMC ID: 3923834
                PubMed ID: 24551153
                SO-VID: de190b17-c6f3-45b9-ba95-0fd6134c8d7f
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