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      • Record: found
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      Type I IFN family members: Similarity, differences and interaction

      research-article
      a , b , a , b , *
      Cytokine & Growth Factor Reviews
      Elsevier Ltd.
      ADAR1, adenosine deaminase acting on RNA 1, AP-1, activator protein 1, APCs, antigen presenting cells, ATF6, activating transcription factor 6, BCG, bacille Calmette–Guérin, cGAS, cyclic GMP-AMP synthase, CHIKV, Chickungunya virus, CRF2, class II cytokine receptor family, ds, double strand, EAE, experimental allergic encephalomyelitis, EM, environmental mycobacteria, EMCV, encephalomyocarditis virus, GAS, gamma interferon activation site, hCMV, human Cytomegalovirus, HCV, hepatitis C virus, HSE, herpes simplex encephalitis, HSV-1, herpes simplex virus-1, IFI16, gamma-interferon-inducible protein 16, IFN, interferon, IFNAR, interferon alpha receptor, IFNGR, interferon gamma receptor, IL, interleukin, IPS-1, interferon promoter-stimulating factor 1, IRAK-4, interleukin-1 receptor-associated kinase 4, IRF, interferon regulatory factor, ISGF3, interferon-stimulated gene factor 3, ISRE, interferon stimulated response element, JAK, Janus kinase, LASV, Lassa virus, MAPK, mitogen-activated protein kinases, MDA5, melanoma differentiation-associated protein 5, MHC, major histocompatibility complex, MS, multiple sclerosis, MSMD, Mendelian susceptibility to mycobacterial disease, MxA, Myxovirus Resistance Gene A, NEMO, nuclear factor (NF)-kB essential modulator, NF-κB, nuclear factor kappa-light-chain-enhancer of activated B cells, NK, natural killer cells, OAS, 2′,5′-oligo adenylate synthetase A, p300/CBP, chromatin remodeling associated p300/CREB-binding protein, PD-L1, programmed death ligand 1, PKR, dsRNA-dependent protein kinase, PRRs, pattern-recognition receptors, RIG-1, retinoic-acid-inducible gene 1, SAMHD1, SAM domain and HD domain-containing protein 1, SARS, severe acute respiratory syndrome, SARS-CoV, severe acute respiratory syndrome-associated coronavirus, SNPs, single nucleotide polymorphisms, SOCS, suppressor of cytokine signaling, ss, single strand, STAT, Signal Transducer and Activator of Transcription, Th, lymphocytes T helper, TLR, Toll-like receptor, TREX1, three prime repair exonuclease 1, TYK2, tyrosine kinase 2, VSV, vesicular stomatitis virus, VZV, Varicella-Zoster virus, WNV, West Nile virus, Interferon types I–III, Interferon genes and receptors, Interferon–interferon interactions, Anti-interferon strategies

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          Abstract

          Interferons (IFN) are key cytokines with multifaceted antiviral and cell-modulatory properties. Three distinct types of IFN are recognized (I–III) based on structural features, receptor usage, cellular source and biological activities. The action of IFNs is mediated by a complex, partially overlapping, transcriptional program initiated by the interaction with specific receptors. Genetic diversity, with polymorphisms and mutations, can modulate the extent of IFN responses and the susceptibility to infections. Almost all viruses developed mechanisms to subvert the IFN response, involving both IFN induction and effector mechanisms. Interactions between IFN types may occur, for both antiviral and cell-modulatory effects, in a complex interplay, involving both synergistic and antagonistic effects. Interferon-associated diseases, not related to virus infections may occur, some of them frequently observed in IFN-treated patients. On the whole, IFNs are pleiotropic biologic response modifiers, that, upon activation of thousands genes, induce a broad spectrum of activities, regulating cell cycle, differentiation, plasma membrane molecules, release of mediators, etc., that can be relevant for cell proliferation, innate and adaptive immunity, hematopoiesis, angiogenesis and other body functions.

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          Most cited references89

          • Record: found
          • Abstract: found
          • Article: not found

          Antiviral actions of interferons.

          C Samuel (2001)
          Tremendous progress has been made in understanding the molecular basis of the antiviral actions of interferons (IFNs), as well as strategies evolved by viruses to antagonize the actions of IFNs. Furthermore, advances made while elucidating the IFN system have contributed significantly to our understanding in multiple areas of virology and molecular cell biology, ranging from pathways of signal transduction to the biochemical mechanisms of transcriptional and translational control to the molecular basis of viral pathogenesis. IFNs are approved therapeutics and have moved from the basic research laboratory to the clinic. Among the IFN-induced proteins important in the antiviral actions of IFNs are the RNA-dependent protein kinase (PKR), the 2',5'-oligoadenylate synthetase (OAS) and RNase L, and the Mx protein GTPases. Double-stranded RNA plays a central role in modulating protein phosphorylation and RNA degradation catalyzed by the IFN-inducible PKR kinase and the 2'-5'-oligoadenylate-dependent RNase L, respectively, and also in RNA editing by the IFN-inducible RNA-specific adenosine deaminase (ADAR1). IFN also induces a form of inducible nitric oxide synthase (iNOS2) and the major histocompatibility complex class I and II proteins, all of which play important roles in immune response to infections. Several additional genes whose expression profiles are altered in response to IFN treatment and virus infection have been identified by microarray analyses. The availability of cDNA and genomic clones for many of the components of the IFN system, including IFN-alpha, IFN-beta, and IFN-gamma, their receptors, Jak and Stat and IRF signal transduction components, and proteins such as PKR, 2',5'-OAS, Mx, and ADAR, whose expression is regulated by IFNs, has permitted the generation of mutant proteins, cells that overexpress different forms of the proteins, and animals in which their expression has been disrupted by targeted gene disruption. The use of these IFN system reagents, both in cell culture and in whole animals, continues to provide important contributions to our understanding of the virus-host interaction and cellular antiviral response.
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            IFN-lambdas mediate antiviral protection through a distinct class II cytokine receptor complex.

            We report here the identification of a ligand-receptor system that, upon engagement, leads to the establishment of an antiviral state. Three closely positioned genes on human chromosome 19 encode distinct but paralogous proteins, which we designate interferon-lambda1 (IFN-lambda1), IFN-lambda2 and IFN-lambda3 (tentatively designated as IL-29, IL-28A and IL-28B, respectively, by HUGO). The expression of IFN-lambda mRNAs was inducible by viral infection in several cell lines. We identified a distinct receptor complex that is utilized by all three IFN-lambda proteins for signaling and is composed of two subunits, a receptor designated CRF2-12 (also designated as IFN-lambdaR1) and a second subunit, CRF2-4 (also known as IL-10R2). Both receptor chains are constitutively expressed on a wide variety of human cell lines and tissues and signal through the Jak-STAT (Janus kinases-signal transducers and activators of transcription) pathway. This receptor-ligand system may contribute to antiviral or other defenses by a mechanism similar to, but independent of, type I IFNs.
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              • Record: found
              • Abstract: found
              • Article: not found

              IL-28, IL-29 and their class II cytokine receptor IL-28R.

              Cytokines play a critical role in modulating the innate and adaptive immune systems. Here, we have identified from the human genomic sequence a family of three cytokines, designated interleukin 28A (IL-28A), IL-28B and IL-29, that are distantly related to type I interferons (IFNs) and the IL-10 family. We found that like type I IFNs, IL-28 and IL-29 were induced by viral infection and showed antiviral activity. However, IL-28 and IL-29 interacted with a heterodimeric class II cytokine receptor that consisted of IL-10 receptor beta (IL-10Rbeta) and an orphan class II receptor chain, designated IL-28Ralpha. This newly described cytokine family may serve as an alternative to type I IFNs in providing immunity to viral infection.
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                Author and article information

                Contributors
                Journal
                Cytokine Growth Factor Rev
                Cytokine Growth Factor Rev
                Cytokine & Growth Factor Reviews
                Elsevier Ltd.
                1359-6101
                1879-0305
                31 October 2014
                April 2015
                31 October 2014
                : 26
                : 2
                : 103-111
                Affiliations
                [a ]Laboratory of Virology, National Institute for Infectious Diseases “L. Spallanzani”, Via Portuense 292, Rome, Italy
                [b ]Department of Biomedical Sciences, University of Sassari, Sassari, Italy
                Author notes
                [* ]Corresponding author at: Department of Biomedical Sciences, University of Sassari, viale San Pietro 42B, 07100 Sassari, Italy. Tel.: +39 3204299685; fax: +39 079212345. doleivir@ 123456uniss.it
                Article
                S1359-6101(14)00139-7
                10.1016/j.cytogfr.2014.10.011
                7108279
                25466633
                da12e7d5-94dd-4679-a230-2908b2dea27d
                Copyright © 2014 Elsevier Ltd. All rights reserved.

                Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.

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                Molecular biology
                adar1, adenosine deaminase acting on rna 1,ap-1, activator protein 1,apcs, antigen presenting cells,atf6, activating transcription factor 6,bcg, bacille calmette–guérin,cgas, cyclic gmp-amp synthase,chikv, chickungunya virus,crf2, class ii cytokine receptor family,ds, double strand,eae, experimental allergic encephalomyelitis,em, environmental mycobacteria,emcv, encephalomyocarditis virus,gas, gamma interferon activation site,hcmv, human cytomegalovirus,hcv, hepatitis c virus,hse, herpes simplex encephalitis,hsv-1, herpes simplex virus-1,ifi16, gamma-interferon-inducible protein 16,ifn, interferon,ifnar, interferon alpha receptor,ifngr, interferon gamma receptor,il, interleukin,ips-1, interferon promoter-stimulating factor 1,irak-4, interleukin-1 receptor-associated kinase 4,irf, interferon regulatory factor,isgf3, interferon-stimulated gene factor 3,isre, interferon stimulated response element,jak, janus kinase,lasv, lassa virus,mapk, mitogen-activated protein kinases,mda5, melanoma differentiation-associated protein 5,mhc, major histocompatibility complex,ms, multiple sclerosis,msmd, mendelian susceptibility to mycobacterial disease,mxa, myxovirus resistance gene a,nemo, nuclear factor (nf)-kb essential modulator,nf-κb, nuclear factor kappa-light-chain-enhancer of activated b cells,nk, natural killer cells,oas, 2′,5′-oligo adenylate synthetase a,p300/cbp, chromatin remodeling associated p300/creb-binding protein,pd-l1, programmed death ligand 1,pkr, dsrna-dependent protein kinase,prrs, pattern-recognition receptors,rig-1, retinoic-acid-inducible gene 1,samhd1, sam domain and hd domain-containing protein 1,sars, severe acute respiratory syndrome,sars-cov, severe acute respiratory syndrome-associated coronavirus,snps, single nucleotide polymorphisms,socs, suppressor of cytokine signaling,ss, single strand,stat, signal transducer and activator of transcription,th, lymphocytes t helper,tlr, toll-like receptor,trex1, three prime repair exonuclease 1,tyk2, tyrosine kinase 2,vsv, vesicular stomatitis virus,vzv, varicella-zoster virus,wnv, west nile virus,interferon types i–iii,interferon genes and receptors,interferon–interferon interactions,anti-interferon strategies
                Molecular biology
                adar1, adenosine deaminase acting on rna 1, ap-1, activator protein 1, apcs, antigen presenting cells, atf6, activating transcription factor 6, bcg, bacille calmette–guérin, cgas, cyclic gmp-amp synthase, chikv, chickungunya virus, crf2, class ii cytokine receptor family, ds, double strand, eae, experimental allergic encephalomyelitis, em, environmental mycobacteria, emcv, encephalomyocarditis virus, gas, gamma interferon activation site, hcmv, human cytomegalovirus, hcv, hepatitis c virus, hse, herpes simplex encephalitis, hsv-1, herpes simplex virus-1, ifi16, gamma-interferon-inducible protein 16, ifn, interferon, ifnar, interferon alpha receptor, ifngr, interferon gamma receptor, il, interleukin, ips-1, interferon promoter-stimulating factor 1, irak-4, interleukin-1 receptor-associated kinase 4, irf, interferon regulatory factor, isgf3, interferon-stimulated gene factor 3, isre, interferon stimulated response element, jak, janus kinase, lasv, lassa virus, mapk, mitogen-activated protein kinases, mda5, melanoma differentiation-associated protein 5, mhc, major histocompatibility complex, ms, multiple sclerosis, msmd, mendelian susceptibility to mycobacterial disease, mxa, myxovirus resistance gene a, nemo, nuclear factor (nf)-kb essential modulator, nf-κb, nuclear factor kappa-light-chain-enhancer of activated b cells, nk, natural killer cells, oas, 2′,5′-oligo adenylate synthetase a, p300/cbp, chromatin remodeling associated p300/creb-binding protein, pd-l1, programmed death ligand 1, pkr, dsrna-dependent protein kinase, prrs, pattern-recognition receptors, rig-1, retinoic-acid-inducible gene 1, samhd1, sam domain and hd domain-containing protein 1, sars, severe acute respiratory syndrome, sars-cov, severe acute respiratory syndrome-associated coronavirus, snps, single nucleotide polymorphisms, socs, suppressor of cytokine signaling, ss, single strand, stat, signal transducer and activator of transcription, th, lymphocytes t helper, tlr, toll-like receptor, trex1, three prime repair exonuclease 1, tyk2, tyrosine kinase 2, vsv, vesicular stomatitis virus, vzv, varicella-zoster virus, wnv, west nile virus, interferon types i–iii, interferon genes and receptors, interferon–interferon interactions, anti-interferon strategies

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