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  • 1
    Keywords: PATHWAY ; GENES ; cell line ; INFECTION ; innate immunity ; HEPATITIS-C VIRUS ; MEMBRANE-PROTEINS ; INDEPENDENT ANTIVIRAL RESPONSE ; IFN-LAMBDA-S ; DENGUE VIRUS
    Abstract: Type I interferon responses are considered the primary means by which viral infections are controlled in mammals. Despite this view, several pathogens activate antiviral responses in the absence of type I interferons. The mechanisms controlling type I interferon-independent responses are undefined. We found that RIG-I like receptors (RLRs) induce type III interferon expression in a variety of human cell types, and identified factors that differentially regulate expression of type I and type III interferons. We identified peroxisomes as a primary site of initiation of type III interferon expression, and revealed that the process of intestinal epithelial cell differentiation upregulates peroxisome biogenesis and promotes robust type III interferon responses in human cells. These findings highlight the importance of different intracellular organelles in specific innate immune responses.
    Type of Publication: Journal article published
    PubMed ID: 24952503
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  • 2
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Gene 135 (1993), S. 161-166 
    ISSN: 0378-1119
    Keywords: Recombinant DNA ; copy-choice model ; direct repeats ; genome rearrangement ; hot spot ; ori ; pausing ; replication fork ; rolling circle ; transposon excision
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology
    Type of Medium: Electronic Resource
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  • 3
    Publication Date: 2011-01-22
    Description: Intracellular pathogens such as Listeria monocytogenes subvert cellular functions through the interaction of bacterial effectors with host components. Here we found that a secreted listerial virulence factor, LntA, could target the chromatin repressor BAHD1 in the host cell nucleus to activate interferon (IFN)-stimulated genes (ISGs). IFN-lambda expression was induced in response to infection of epithelial cells with bacteria lacking LntA; however, the BAHD1-chromatin associated complex repressed downstream ISGs. In contrast, in cells infected with lntA-expressing bacteria, LntA prevented BAHD1 recruitment to ISGs and stimulated their expression. Murine listeriosis decreased in BAHD1(+/-) mice or when lntA was constitutively expressed. Thus, the LntA-BAHD1 interplay may modulate IFN-lambda-mediated immune response to control bacterial colonization of the host.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lebreton, Alice -- Lakisic, Goran -- Job, Viviana -- Fritsch, Lauriane -- Tham, To Nam -- Camejo, Ana -- Mattei, Pierre-Jean -- Regnault, Beatrice -- Nahori, Marie-Anne -- Cabanes, Didier -- Gautreau, Alexis -- Ait-Si-Ali, Slimane -- Dessen, Andrea -- Cossart, Pascale -- Bierne, Helene -- 233348/European Research Council/International -- New York, N.Y. -- Science. 2011 Mar 11;331(6022):1319-21. doi: 10.1126/science.1200120. Epub 2011 Jan 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut Pasteur, Unite des Interactions Bacteries Cellules, Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21252314" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Line ; Cell Line, Tumor ; Cell Nucleus/metabolism ; Chromatin/*metabolism ; Chromosomal Proteins, Non-Histone/*metabolism ; Down-Regulation ; Gene Expression Profiling ; Gene Expression Regulation ; Host-Pathogen Interactions ; Humans ; Interferons/genetics/immunology/*metabolism ; Interleukins/genetics/immunology/*metabolism ; Listeria monocytogenes/genetics/metabolism/*pathogenicity ; Listeriosis/*immunology/microbiology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Molecular Sequence Data ; Signal Transduction ; Virulence Factors/chemistry/genetics/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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