Interferon Lambda: Modulating Immunity in Infectious Diseases
Identifieur interne : 000766 ( Pmc/Curation ); précédent : 000765; suivant : 000767Interferon Lambda: Modulating Immunity in Infectious Diseases
Auteurs : Mohammedyaseen Syedbasha [Suisse] ; Adrian Egli [Suisse]Source :
- Frontiers in Immunology [ 1664-3224 ] ; 2017.
Abstract
Interferon lambdas (IFN-λs; IFNL1-4) modulate immunity in the context of infections and autoimmune diseases, through a network of induced genes. IFN-λs act by binding to the heterodimeric IFN-λ receptor (IFNLR), activating a STAT phosphorylation-dependent signaling cascade. Thereby hundreds of IFN-stimulated genes are induced, which modulate various immune functions
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DOI: 10.3389/fimmu.2017.00119
PubMed: 28293236
PubMed Central: 5328987
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Interferon Lambda: Modulating Immunity in Infectious Diseases</title><author><name sortKey="Syedbasha, Mohammedyaseen" sort="Syedbasha, Mohammedyaseen" uniqKey="Syedbasha M" first="Mohammedyaseen" last="Syedbasha">Mohammedyaseen Syedbasha</name><affiliation wicri:level="1"><nlm:aff id="aff1"><institution>Applied Microbiology Research, Department of Biomedicine, University of Basel</institution>,<addr-line>Basel</addr-line>,<country>Switzerland</country></nlm:aff><country xml:lang="fr">Suisse</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Egli, Adrian" sort="Egli, Adrian" uniqKey="Egli A" first="Adrian" last="Egli">Adrian Egli</name><affiliation wicri:level="1"><nlm:aff id="aff1"><institution>Applied Microbiology Research, Department of Biomedicine, University of Basel</institution>,<addr-line>Basel</addr-line>,<country>Switzerland</country></nlm:aff><country xml:lang="fr">Suisse</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="aff2"><institution>Clinical Microbiology, University Hospital Basel</institution>,<addr-line>Basel</addr-line>,<country>Switzerland</country></nlm:aff><country xml:lang="fr">Suisse</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">28293236</idno><idno type="pmc">5328987</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5328987</idno><idno type="RBID">PMC:5328987</idno><idno type="doi">10.3389/fimmu.2017.00119</idno><date when="2017">2017</date><idno type="wicri:Area/Pmc/Corpus">000766</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000766</idno><idno type="wicri:Area/Pmc/Curation">000766</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">000766</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Interferon Lambda: Modulating Immunity in Infectious Diseases</title><author><name sortKey="Syedbasha, Mohammedyaseen" sort="Syedbasha, Mohammedyaseen" uniqKey="Syedbasha M" first="Mohammedyaseen" last="Syedbasha">Mohammedyaseen Syedbasha</name><affiliation wicri:level="1"><nlm:aff id="aff1"><institution>Applied Microbiology Research, Department of Biomedicine, University of Basel</institution>,<addr-line>Basel</addr-line>,<country>Switzerland</country></nlm:aff><country xml:lang="fr">Suisse</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Egli, Adrian" sort="Egli, Adrian" uniqKey="Egli A" first="Adrian" last="Egli">Adrian Egli</name><affiliation wicri:level="1"><nlm:aff id="aff1"><institution>Applied Microbiology Research, Department of Biomedicine, University of Basel</institution>,<addr-line>Basel</addr-line>,<country>Switzerland</country></nlm:aff><country xml:lang="fr">Suisse</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="aff2"><institution>Clinical Microbiology, University Hospital Basel</institution>,<addr-line>Basel</addr-line>,<country>Switzerland</country></nlm:aff><country xml:lang="fr">Suisse</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author></analytic><series><title level="j">Frontiers in Immunology</title><idno type="eISSN">1664-3224</idno><imprint><date when="2017">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Interferon lambdas (IFN-λs; IFNL1-4) modulate immunity in the context of infections and autoimmune diseases, through a network of induced genes. IFN-λs act by binding to the heterodimeric IFN-λ receptor (IFNLR), activating a STAT phosphorylation-dependent signaling cascade. Thereby hundreds of IFN-stimulated genes are induced, which modulate various immune functions <italic>via</italic> complex forward and feedback loops. When compared to the well-characterized IFN-α signaling cascade, three important differences have been discovered. First, the IFNLR is not ubiquitously expressed: in particular, immune cells show significant variation in the expression levels of and susceptibilities to IFN-λs. Second, the binding affinities of individual IFN-λs to the IFNLR varies greatly and are generally lower compared to the binding affinities of IFN-α to its receptor. Finally, genetic variation in the form of a series of single-nucleotide polymorphisms (SNPs) linked to genes involved in the IFN-λ signaling cascade has been described and associated with the clinical course and treatment outcomes of hepatitis B and C virus infection. The clinical impact of IFN-λ signaling and the SNP variations may, however, reach far beyond viral hepatitis. Recent publications show important roles for IFN-λs in a broad range of viral infections such as human T-cell leukemia type-1 virus, rotaviruses, and influenza virus. IFN-λ also potentially modulates the course of bacterial colonization and infections as shown for <italic>Staphylococcus aureus</italic> and <italic>Mycobacterium tuberculosis</italic>. Although the immunological processes involved in controlling viral and bacterial infections are distinct, IFN-λs may interfere at various levels: as an innate immune cytokine with direct antiviral effects; or as a modulator of IFN-α-induced signaling <italic>via</italic> the suppressor of cytokine signaling 1 and the ubiquitin-specific peptidase 18 inhibitory feedback loops. In addition, the modulation of adaptive immune functions <italic>via</italic> macrophage and dendritic cell polarization, and subsequent priming, activation, and proliferation of pathogen-specific T- and B-cells may also be important elements associated with infectious disease outcomes. This review summarizes the emerging details of the IFN-λ immunobiology in the context of the host immune response and viral and bacterial infections.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Bowness, R" uniqKey="Bowness R">R Bowness</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Subramanian, N" uniqKey="Subramanian N">N Subramanian</name></author><author><name sortKey="Torabi Parizi, P" uniqKey="Torabi Parizi P">P Torabi-Parizi</name></author><author><name sortKey="Gottschalk, Ra" uniqKey="Gottschalk R">RA Gottschalk</name></author><author><name sortKey="Germain, Rn" uniqKey="Germain R">RN Germain</name></author><author><name sortKey="Dutta, B" uniqKey="Dutta B">B Dutta</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Tsang, Js" uniqKey="Tsang J">JS Tsang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Linnik, Je" 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<front><journal-meta><journal-id journal-id-type="nlm-ta">Front Immunol</journal-id><journal-id journal-id-type="iso-abbrev">Front Immunol</journal-id><journal-id journal-id-type="publisher-id">Front. Immunol.</journal-id><journal-title-group><journal-title>Frontiers in Immunology</journal-title></journal-title-group><issn pub-type="epub">1664-3224</issn><publisher><publisher-name>Frontiers Media S.A.</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">28293236</article-id><article-id pub-id-type="pmc">5328987</article-id><article-id pub-id-type="doi">10.3389/fimmu.2017.00119</article-id><article-categories><subj-group subj-group-type="heading"><subject>Immunology</subject><subj-group><subject>Review</subject></subj-group></subj-group></article-categories><title-group><article-title>Interferon Lambda: Modulating Immunity in Infectious Diseases</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Syedbasha</surname><given-names>Mohammedyaseen</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref><uri xlink:type="simple" xlink:href="http://frontiersin.org/people/u/415944"></uri></contrib><contrib contrib-type="author"><name><surname>Egli</surname><given-names>Adrian</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref><xref ref-type="aff" rid="aff2"><sup>2</sup></xref><xref ref-type="corresp" rid="cor1">*</xref><uri xlink:type="simple" xlink:href="http://frontiersin.org/people/u/362316"></uri></contrib></contrib-group><aff id="aff1"><sup>1</sup><institution>Applied Microbiology Research, Department of Biomedicine, University of Basel</institution>,<addr-line>Basel</addr-line>,<country>Switzerland</country></aff><aff id="aff2"><sup>2</sup><institution>Clinical Microbiology, University Hospital Basel</institution>,<addr-line>Basel</addr-line>,<country>Switzerland</country></aff><author-notes><fn fn-type="edited-by"><p>Edited by: Claudia U. Duerr, McGill University, Canada</p></fn><fn fn-type="edited-by"><p>Reviewed by: TImothy Nice, Oregon Health & Science University, USA; Megan Tierney Baldridge, Washington University School of Medicine, USA; Charlotte Odendall, King’s College London, UK</p></fn><corresp content-type="corresp" id="cor1">*Correspondence: Adrian Egli, <email>adrian.egli@usb.ch</email></corresp><fn fn-type="other" id="fn002"><p>Specialty section: This article was submitted to Molecular Innate Immunity, a section of the journal Frontiers in Immunology</p></fn></author-notes><pub-date pub-type="epub"><day>28</day><month>2</month><year>2017</year></pub-date><pub-date pub-type="collection"><year>2017</year></pub-date><volume>8</volume><elocation-id>119</elocation-id><history><date date-type="received"><day>12</day><month>11</month><year>2016</year></date><date date-type="accepted"><day>25</day><month>1</month><year>2017</year></date></history><permissions><copyright-statement>Copyright © 2017 Syedbasha and Egli.</copyright-statement><copyright-year>2017</copyright-year><copyright-holder>Syedbasha and Egli</copyright-holder><license xlink:href="http://creativecommons.org/licenses/by/4.0/"><license-p>This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.</license-p></license></permissions><abstract><p>Interferon lambdas (IFN-λs; IFNL1-4) modulate immunity in the context of infections and autoimmune diseases, through a network of induced genes. IFN-λs act by binding to the heterodimeric IFN-λ receptor (IFNLR), activating a STAT phosphorylation-dependent signaling cascade. Thereby hundreds of IFN-stimulated genes are induced, which modulate various immune functions <italic>via</italic> complex forward and feedback loops. When compared to the well-characterized IFN-α signaling cascade, three important differences have been discovered. First, the IFNLR is not ubiquitously expressed: in particular, immune cells show significant variation in the expression levels of and susceptibilities to IFN-λs. Second, the binding affinities of individual IFN-λs to the IFNLR varies greatly and are generally lower compared to the binding affinities of IFN-α to its receptor. Finally, genetic variation in the form of a series of single-nucleotide polymorphisms (SNPs) linked to genes involved in the IFN-λ signaling cascade has been described and associated with the clinical course and treatment outcomes of hepatitis B and C virus infection. The clinical impact of IFN-λ signaling and the SNP variations may, however, reach far beyond viral hepatitis. Recent publications show important roles for IFN-λs in a broad range of viral infections such as human T-cell leukemia type-1 virus, rotaviruses, and influenza virus. IFN-λ also potentially modulates the course of bacterial colonization and infections as shown for <italic>Staphylococcus aureus</italic> and <italic>Mycobacterium tuberculosis</italic>. Although the immunological processes involved in controlling viral and bacterial infections are distinct, IFN-λs may interfere at various levels: as an innate immune cytokine with direct antiviral effects; or as a modulator of IFN-α-induced signaling <italic>via</italic> the suppressor of cytokine signaling 1 and the ubiquitin-specific peptidase 18 inhibitory feedback loops. In addition, the modulation of adaptive immune functions <italic>via</italic> macrophage and dendritic cell polarization, and subsequent priming, activation, and proliferation of pathogen-specific T- and B-cells may also be important elements associated with infectious disease outcomes. This review summarizes the emerging details of the IFN-λ immunobiology in the context of the host immune response and viral and bacterial infections.</p></abstract><kwd-group><kwd>interferon lambda</kwd><kwd>immunity</kwd><kwd>immune cells</kwd><kwd>virus</kwd><kwd>infectious diseases</kwd><kwd>bacteria</kwd><kwd>fungi</kwd><kwd>parasites</kwd></kwd-group><funding-group><award-group><funding-source id="cn01">Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung<named-content content-type="fundref-id">10.13039/501100001711</named-content></funding-source><award-id rid="cn01">PZ00P3_154709</award-id></award-group></funding-group><counts><fig-count count="2"></fig-count><table-count count="2"></table-count><equation-count count="0"></equation-count><ref-count count="182"></ref-count><page-count count="13"></page-count><word-count count="11431"></word-count></counts></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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