Altered RIG-I/DDX58-mediated innate immunity in dermatomyositis
We investigated the molecular mechanisms involved in the pathogenesis of three inflammatory myopathies, dermatomyositis (DM), polymyositis (PM) and inclusion body myositis (IBM). We performed microarray experiments† using microdissected pathological muscle fibres from 15 patients with these disorder...
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| Published in | The Journal of pathology Vol. 233; no. 3; pp. 258 - 268 |
|---|---|
| Main Authors | , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Chichester, UK
John Wiley & Sons, Ltd
01.07.2014
Wiley Subscription Services, Inc |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0022-3417 1096-9896 1096-9896 |
| DOI | 10.1002/path.4346 |
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| Abstract | We investigated the molecular mechanisms involved in the pathogenesis of three inflammatory myopathies, dermatomyositis (DM), polymyositis (PM) and inclusion body myositis (IBM). We performed microarray experiments† using microdissected pathological muscle fibres from 15 patients with these disorders and five controls. Differentially expressed candidate genes were validated by immunohistochemistry on muscle biopsies, and the altered pathways were analysed in human myotube cultures. Up‐regulation of genes involved in viral and nucleic acid recognition were found in the three myopathies but not in controls. In DM, retinoic acid‐inducible gene 1 (RIG‐I, DDX58) and the novel antiviral factor DDX60, which promotes RIG‐I‐mediated signalling, were significantly up‐regulated, followed by IFIH1 (MDA5) and TLR3. Immunohistochemistry confirmed over‐expression of RIG‐I in pathological muscle fibres in 5/5 DM, 0/5 PM and 0/5 IBM patients, and in 0/5 controls. Stimulation of human myotubes with a ligand of RIG‐I produced a significant secretion of interferon‐β (IFNβ; p < 0.05) and up‐regulation of class I MHC, RIG‐I and TLR3 (p < 0.05) by IFNβ‐dependent and TLR3‐independent mechanisms. RIG‐I‐mediated innate immunity, triggered by a viral or damage signal, plays a significant role in the pathogenesis of DM, but not in that of PM or IBM. Copyright © 2014 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd |
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| AbstractList | We investigated the molecular mechanisms involved in the pathogenesis of three inflammatory myopathies, dermatomyositis (DM), polymyositis (PM) and inclusion body myositis (IBM). We performed microarray experiments super() using microdissected pathological muscle fibres from 15 patients with these disorders and five controls. Differentially expressed candidate genes were validated by immunohistochemistry on muscle biopsies, and the altered pathways were analysed in human myotube cultures. Up-regulation of genes involved in viral and nucleic acid recognition were found in the three myopathies but not in controls. In DM, retinoic acid-inducible gene 1 ( RIG-I , DDX58 ) and the novel antiviral factor DDX60 , which promotes RIG-I-mediated signalling, were significantly up-regulated, followed by IFIH1 ( MDA5 ) and TLR3 . Immunohistochemistry confirmed over-expression of RIG-I in pathological muscle fibres in 5/5 DM, 0/5 PM and 0/5 IBM patients, and in 0/5 controls. Stimulation of human myotubes with a ligand of RIG-I produced a significant secretion of interferon- [beta] (IFN [beta] ; p < 0.05) and up-regulation of class I MHC, RIG-I and TLR3 ( p < 0.05) by IFN [beta] -dependent and TLR3-independent mechanisms. RIG-I-mediated innate immunity, triggered by a viral or damage signal, plays a significant role in the pathogenesis of DM, but not in that of PM or IBM. Copyright copyright 2014 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd We investigated the molecular mechanisms involved in the pathogenesis of three inflammatory myopathies, dermatomyositis (DM), polymyositis (PM) and inclusion body myositis (IBM). We performed microarray experiments(†) using microdissected pathological muscle fibres from 15 patients with these disorders and five controls. Differentially expressed candidate genes were validated by immunohistochemistry on muscle biopsies, and the altered pathways were analysed in human myotube cultures. Up-regulation of genes involved in viral and nucleic acid recognition were found in the three myopathies but not in controls. In DM, retinoic acid-inducible gene 1 (RIG-I, DDX58) and the novel antiviral factor DDX60, which promotes RIG-I-mediated signalling, were significantly up-regulated, followed by IFIH1 (MDA5) and TLR3. Immunohistochemistry confirmed over-expression of RIG-I in pathological muscle fibres in 5/5 DM, 0/5 PM and 0/5 IBM patients, and in 0/5 controls. Stimulation of human myotubes with a ligand of RIG-I produced a significant secretion of interferon-β (IFNβ; p < 0.05) and up-regulation of class I MHC, RIG-I and TLR3 (p < 0.05) by IFNβ-dependent and TLR3-independent mechanisms. RIG-I-mediated innate immunity, triggered by a viral or damage signal, plays a significant role in the pathogenesis of DM, but not in that of PM or IBM. We investigated the molecular mechanisms involved in the pathogenesis of three inflammatory myopathies, dermatomyositis (DM), polymyositis (PM) and inclusion body myositis (IBM). We performed microarray experiments† using microdissected pathological muscle fibres from 15 patients with these disorders and five controls. Differentially expressed candidate genes were validated by immunohistochemistry on muscle biopsies, and the altered pathways were analysed in human myotube cultures. Up‐regulation of genes involved in viral and nucleic acid recognition were found in the three myopathies but not in controls. In DM, retinoic acid‐inducible gene 1 (RIG‐I, DDX58) and the novel antiviral factor DDX60, which promotes RIG‐I‐mediated signalling, were significantly up‐regulated, followed by IFIH1 (MDA5) and TLR3. Immunohistochemistry confirmed over‐expression of RIG‐I in pathological muscle fibres in 5/5 DM, 0/5 PM and 0/5 IBM patients, and in 0/5 controls. Stimulation of human myotubes with a ligand of RIG‐I produced a significant secretion of interferon‐β (IFNβ; p < 0.05) and up‐regulation of class I MHC, RIG‐I and TLR3 (p < 0.05) by IFNβ‐dependent and TLR3‐independent mechanisms. RIG‐I‐mediated innate immunity, triggered by a viral or damage signal, plays a significant role in the pathogenesis of DM, but not in that of PM or IBM. Copyright © 2014 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd We investigated the molecular mechanisms involved in the pathogenesis of three inflammatory myopathies, dermatomyositis (DM), polymyositis (PM) and inclusion body myositis (IBM). We performed microarray experiments(†) using microdissected pathological muscle fibres from 15 patients with these disorders and five controls. Differentially expressed candidate genes were validated by immunohistochemistry on muscle biopsies, and the altered pathways were analysed in human myotube cultures. Up-regulation of genes involved in viral and nucleic acid recognition were found in the three myopathies but not in controls. In DM, retinoic acid-inducible gene 1 (RIG-I, DDX58) and the novel antiviral factor DDX60, which promotes RIG-I-mediated signalling, were significantly up-regulated, followed by IFIH1 (MDA5) and TLR3. Immunohistochemistry confirmed over-expression of RIG-I in pathological muscle fibres in 5/5 DM, 0/5 PM and 0/5 IBM patients, and in 0/5 controls. Stimulation of human myotubes with a ligand of RIG-I produced a significant secretion of interferon-β (IFNβ; p < 0.05) and up-regulation of class I MHC, RIG-I and TLR3 (p < 0.05) by IFNβ-dependent and TLR3-independent mechanisms. RIG-I-mediated innate immunity, triggered by a viral or damage signal, plays a significant role in the pathogenesis of DM, but not in that of PM or IBM.We investigated the molecular mechanisms involved in the pathogenesis of three inflammatory myopathies, dermatomyositis (DM), polymyositis (PM) and inclusion body myositis (IBM). We performed microarray experiments(†) using microdissected pathological muscle fibres from 15 patients with these disorders and five controls. Differentially expressed candidate genes were validated by immunohistochemistry on muscle biopsies, and the altered pathways were analysed in human myotube cultures. Up-regulation of genes involved in viral and nucleic acid recognition were found in the three myopathies but not in controls. In DM, retinoic acid-inducible gene 1 (RIG-I, DDX58) and the novel antiviral factor DDX60, which promotes RIG-I-mediated signalling, were significantly up-regulated, followed by IFIH1 (MDA5) and TLR3. Immunohistochemistry confirmed over-expression of RIG-I in pathological muscle fibres in 5/5 DM, 0/5 PM and 0/5 IBM patients, and in 0/5 controls. Stimulation of human myotubes with a ligand of RIG-I produced a significant secretion of interferon-β (IFNβ; p < 0.05) and up-regulation of class I MHC, RIG-I and TLR3 (p < 0.05) by IFNβ-dependent and TLR3-independent mechanisms. RIG-I-mediated innate immunity, triggered by a viral or damage signal, plays a significant role in the pathogenesis of DM, but not in that of PM or IBM. We investigated the molecular mechanisms involved in the pathogenesis of three inflammatory myopathies, dermatomyositis (DM), polymyositis (PM) and inclusion body myositis (IBM). We performed microarray experiments[dagger] using microdissected pathological muscle fibres from 15 patients with these disorders and five controls. Differentially expressed candidate genes were validated by immunohistochemistry on muscle biopsies, and the altered pathways were analysed in human myotube cultures. Up-regulation of genes involved in viral and nucleic acid recognition were found in the three myopathies but not in controls. In DM, retinoic acid-inducible gene 1 (RIG-I, DDX58) and the novel antiviral factor DDX60, which promotes RIG-I-mediated signalling, were significantly up-regulated, followed by IFIH1 (MDA5) and TLR3. Immunohistochemistry confirmed over-expression of RIG-I in pathological muscle fibres in 5/5 DM, 0/5 PM and 0/5 IBM patients, and in 0/5 controls. Stimulation of human myotubes with a ligand of RIG-I produced a significant secretion of interferon-[beta] (IFN[beta]; p < 0.05) and up-regulation of class I MHC, RIG-I and TLR3 (p < 0.05) by IFN[beta]-dependent and TLR3-independent mechanisms. RIG-I-mediated innate immunity, triggered by a viral or damage signal, plays a significant role in the pathogenesis of DM, but not in that of PM or IBM. Copyright © 2014 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd [PUBLICATION ABSTRACT] We investigated the molecular mechanisms involved in the pathogenesis of three inflammatory myopathies, dermatomyositis ( DM ), polymyositis ( PM ) and inclusion body myositis ( IBM ). We performed microarray experiments † using microdissected pathological muscle fibres from 15 patients with these disorders and five controls. Differentially expressed candidate genes were validated by immunohistochemistry on muscle biopsies, and the altered pathways were analysed in human myotube cultures. Up‐regulation of genes involved in viral and nucleic acid recognition were found in the three myopathies but not in controls. In DM , retinoic acid‐inducible gene 1 ( RIG ‐I , DDX58 ) and the novel antiviral factor DDX60 , which promotes RIG ‐I‐mediated signalling, were significantly up‐regulated, followed by IFIH1 ( MDA5 ) and TLR3 . Immunohistochemistry confirmed over‐expression of RIG ‐I in pathological muscle fibres in 5/5 DM , 0/5 PM and 0/5 IBM patients, and in 0/5 controls. Stimulation of human myotubes with a ligand of RIG ‐I produced a significant secretion of interferon‐ β ( IFN β ; p < 0.05) and up‐regulation of class I MHC , RIG ‐I and TLR3 ( p < 0.05) by IFN β ‐dependent and TLR3 ‐independent mechanisms. RIG ‐I‐mediated innate immunity, triggered by a viral or damage signal, plays a significant role in the pathogenesis of DM , but not in that of PM or IBM . Copyright © 2014 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd |
| Author | Díaz-Manera, Jordi Illa, Isabel Gallardo, Eduard Navas, Miquel Suárez-Calvet, Xavier Nogales-Gadea, Gisela Rojas-Garcia, Ricard Querol, Luis |
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| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/24604766$$D View this record in MEDLINE/PubMed |
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| Keywords | RIG-I dermatomyositis innate immunity DDX58 inflammatory myopathy |
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| Notes | Immunoguided laser Microdissection. A representative MHC-I-positive perifascicular area from a DM patient is shown before (A) and after (B) microdissection. Care was taken to avoid microdissection of inflammatory infiltratesIFIH1 (MDA5) is not detected in DM muscle by immunohistochemistry (A), but is present in the sarcoplasm of human control myotubes (B); scale bar = 100 µmHighest differentially up-regulated genes in dermatomyositis ark:/67375/WNG-VJNBH6B3-W ArticleID:PATH4346 istex:E621EE91F9E5B54BBC8434A7B4B577369E90FCCE ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 14 ObjectType-Article-1 ObjectType-Feature-2 content type line 23 |
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| PublicationDateYYYYMMDD | 2014-07-01 |
| PublicationDate_xml | – month: 07 year: 2014 text: July 2014 |
| PublicationDecade | 2010 |
| PublicationPlace | Chichester, UK |
| PublicationPlace_xml | – name: Chichester, UK – name: England – name: Bognor Regis |
| PublicationTitle | The Journal of pathology |
| PublicationTitleAlternate | J. Pathol |
| PublicationYear | 2014 |
| Publisher | John Wiley & Sons, Ltd Wiley Subscription Services, Inc |
| Publisher_xml | – name: John Wiley & Sons, Ltd – name: Wiley Subscription Services, Inc |
| References | Greenberg SA, Pinkus JL, Pinkus GS, et al. Interferon-α/β-mediated innate immune mechanisms in dermatomyositis. Ann Neurol 2005; 57: 664-678. Cappelletti C, Baggi F, Zolezzi F, et al. Type I interferon and Toll-like receptor expression characterizes inflammatory myopathies. Neurology 2011; 76: 2079-2088. Kawai T, Akira S. Toll-like receptor and RIG-I-like receptor signaling. Ann N Y Acad Sci 2008; 1143: 1-20. Dalakas MC. Pathogenesis and therapies of immune-mediated myopathies. Autoimmun Rev 2012; 11: 203-206. Chakrabarti A, Jha BK, Silverman RH. New insights into the role of RNase L in innate immunity. J Interferon Cytokine Res 2011; 31: 49-57. Nagaraju K, Casciola-Rosen L, Lundberg I, et al. Activation of the endoplasmic reticulum stress response in autoimmune myositis: potential role in muscle fiber damage and dysfunction. Arthritis Rheum 2005; 52: 1824-1835. Nagaraju K, Raben N, Loeffler L, et al. Conditional up-regulation of MHC class I in skeletal muscle leads to self-sustaining autoimmune myositis and myositis-specific autoantibodies. Proc Natl Acad Sci USA 2000; 97: 9209-9214. Miyashita M, Oshiumi H, Matsumoto M, et al. DDX60, a DEXD/H box helicase, is a novel antiviral factor promoting RIG-I-like receptor-mediated signaling. Mol Cell Biol 2011; 31: 3802-3819. Seo JY, Yaneva R, Cresswell P. Viperin: a multifunctional, interferon-inducible protein that regulates virus replication. Cell Host Microbe 2011; 10: 534-539. Gallardo E, de Andres I, Illa I. Cathepsins are upregulated by IFN-γ/STAT1 in human muscle culture: a possible active factor in dermatomyositis. J Neuropathol Exp Neurol 2001; 60: 847-855. Smyth GK. Linear models and empirical bayes methods for assessing differential expression in microarray experiments. Stat Appl Genet Mol Biol 2004; 3: article 3. Castanier C, Garcin D, Vazquez A, et al. Mitochondrial dynamics regulate the RIG-I-like receptor antiviral pathway. EMBO Rep 2010; 11: 133-138. Uaesoontrachoon K, Cha HJ, Ampong B, et al. The effects of MyD88 deficiency on disease phenotype in dysferlin-deficient A/J mice: role of endogenous TLR ligands. J Pathol 2013; 231: 199-209. Salajegheh M, Kong SW, Pinkus JL, et al. Interferon-stimulated gene 15 (ISG15) conjugates proteins in dermatomyositis muscle with perifascicular atrophy. Ann Neurol 2010; 67: 53-63. Cufi P, Dragin N, Weiss JM, et al. Implication of double-stranded RNA signaling in the etiology of autoimmune myasthenia gravis. Ann Neurol 2013; 73: 281-293. Nakashima R, Imura Y, Kobayashi S, et al. The RIG-I-like receptor IFIH1/MDA5 is a dermatomyositis-specific autoantigen identified by the anti-CADM-140 antibody. Rheumatology (Oxford) 2010; 49: 433-440. Engel AG, Franzini-Armstrong C. Myology: Basic and Clinical. McGraw-Hill Medical: New York, 2004: 1321-1486. Tournadre A, Lenief V, Eljaafari A, et al. Immature muscle precursors are a source of interferon-β in myositis: role of Toll-like receptor 3 activation and contribution to HLA class I up-regulation. Arthritis Rheum 2012; 64: 533-541. Kuznik A, Bencina M, Svajger U, et al. Mechanism of endosomal TLR inhibition by antimalarial drugs and imidazoquinolines. J Immunol 2011; 186: 4794-4804. Loo YM GMJ. Immune signaling by RIG-I-like receptors. Immunity 2011; 34: 680-692. Dalakas MC, Hohlfeld R. Polymyositis and dermatomyositis. Lancet 2003; 362: 971-982. Larman HB, Salajegheh M, Nazareno R, et al. Cytosolic 5′-nucleotidase 1A autoimmunity in sporadic inclusion body myositis. Ann Neurol 2013; 73: 408-418. D'Cunha J, Knight E, Jr., Haas AL, et al. Immunoregulatory properties of ISG15, an interferon-induced cytokine. Proc Natl Acad Sci USA 1996; 93: 211-215. Kato H, Sato S, Yoneyama M, et al. Cell type-specific involvement of RIG-I in antiviral response. Immunity 2005; 23: 19-28. Salminen A, Kauppinen A, Kaarniranta K. Emerging role of NF-κB signaling in the induction of senescence-associated secretory phenotype (SASP). Cell Signal 2012; 24: 835-845. Li CK, Knopp P, Moncrieffe H, et al. Overexpression of MHC class I heavy chain protein in young skeletal muscle leads to severe myositis: implications for juvenile myositis. Am J Pathol 2009; 175: 1030-1040. Higgs BW, Liu Z, White B, et al. Patients with systemic lupus erythematosus, myositis, rheumatoid arthritis and scleroderma share activation of a common type I interferon pathway. Ann Rheum Dis 2011; 70: 2029-2036. Greenberg SA, Sanoudou D, Haslett JN, et al. Molecular profiles of inflammatory myopathies. Neurology 2002; 59: 1170-1182. Malathi K, Dong B, Gale M, Jr., et al. Small self-RNA generated by RNase L amplifies antiviral innate immunity. Nature 2007; 448: 816-819. Ramos HJ, Gale M Jr. RIG-I like receptors and their signaling crosstalk in the regulation of antiviral immunity. Curr Opin Virol 2011; 1: 167-176. Casciola-Rosen L, Nagaraju K, Plotz P, et al. Enhanced autoantigen expression in regenerating muscle cells in idiopathic inflammatory myopathy. J Exp Med 2005; 201: 591-601. Yasukawa K, Oshiumi H, Takeda M, et al. Mitofusin 2 inhibits mitochondrial antiviral signaling. Sci Signal 2009; 2: ra47. Mammen AL. Autoimmune myopathies: autoantibodies, phenotypes and pathogenesis. Nat Rev Neurol 2011; 7: 343-354. Hornung V, Ellegast J, Kim S, et al. 5'-Triphosphate RNA is the ligand for RIG-I. Science 2006; 314: 994-997. Hinson ER, Cresswell P. The antiviral protein, viperin, localizes to lipid droplets via its N-terminal amphipathic α-helix. Proc Natl Acad Sci USA 2009; 106: 20452-20457. Kim GT, Cho ML, Park YE, et al. Expression of TLR2, TLR4, and TLR9 in dermatomyositis and polymyositis. Clin Rheumatol 2010; 29: 273-279. Illa I, Gallardo E, Gimeno R, et al. Signal transducer and activator of transcription 1 in human muscle: implications in inflammatory myopathies. Am J Pathol 1997; 151: 81-88. De Luna N, Gallardo E, Sonnet C, et al. Role of thrombospondin 1 in macrophage inflammation in dysferlin myopathy. J Neuropathol Exp Neurol 2010; 69: 643-653. de Luna N, Gallardo E, Soriano M, et al. Absence of dysferlin alters myogenin expression and delays human muscle differentiation 'in vitro'. J Biol Chem 2006; 281: 17092-17098. Poeck H, Bscheider M, Gross O, et al. Recognition of RNA virus by RIG-I results in activation of CARD9 and inflammasome signaling for interleukin 1β production. Nat Immunol 2010; 11: 63-69. 2010; 11 2002; 59 2007; 448 2011; 1 1997; 151 2011; 31 1996; 93 2004; 3 2011; 76 2011; 10 2004 2011; 34 2009; 175 2006; 314 2012; 11 2011; 7 2005; 23 2010; 67 2008; 1143 2001; 60 2010; 49 2010; 69 2010; 29 2005; 201 2013; 73 2011; 70 2000; 97 2005; 52 2013; 231 2006; 281 2012; 24 2009; 2 2012; 64 2003; 362 2005; 57 2011; 186 2009; 106 e_1_2_7_6_1 e_1_2_7_5_1 e_1_2_7_4_1 e_1_2_7_3_1 e_1_2_7_9_1 e_1_2_7_8_1 e_1_2_7_7_1 e_1_2_7_19_1 e_1_2_7_18_1 e_1_2_7_17_1 e_1_2_7_16_1 e_1_2_7_40_1 e_1_2_7_15_1 e_1_2_7_41_1 e_1_2_7_14_1 e_1_2_7_13_1 e_1_2_7_12_1 e_1_2_7_11_1 e_1_2_7_10_1 e_1_2_7_26_1 e_1_2_7_27_1 e_1_2_7_28_1 e_1_2_7_29_1 Illa I (e_1_2_7_23_1) 1997; 151 e_1_2_7_30_1 e_1_2_7_25_1 e_1_2_7_31_1 e_1_2_7_24_1 e_1_2_7_32_1 e_1_2_7_33_1 e_1_2_7_22_1 e_1_2_7_34_1 e_1_2_7_21_1 e_1_2_7_35_1 Engel AG (e_1_2_7_2_1) 2004 e_1_2_7_20_1 e_1_2_7_36_1 e_1_2_7_37_1 e_1_2_7_38_1 e_1_2_7_39_1 24687932 - J Pathol. 2014 Jul;233(3):215-6 |
| References_xml | – reference: Cufi P, Dragin N, Weiss JM, et al. Implication of double-stranded RNA signaling in the etiology of autoimmune myasthenia gravis. Ann Neurol 2013; 73: 281-293. – reference: Kato H, Sato S, Yoneyama M, et al. Cell type-specific involvement of RIG-I in antiviral response. Immunity 2005; 23: 19-28. – reference: Seo JY, Yaneva R, Cresswell P. Viperin: a multifunctional, interferon-inducible protein that regulates virus replication. Cell Host Microbe 2011; 10: 534-539. – reference: Ramos HJ, Gale M Jr. RIG-I like receptors and their signaling crosstalk in the regulation of antiviral immunity. Curr Opin Virol 2011; 1: 167-176. – reference: Higgs BW, Liu Z, White B, et al. Patients with systemic lupus erythematosus, myositis, rheumatoid arthritis and scleroderma share activation of a common type I interferon pathway. Ann Rheum Dis 2011; 70: 2029-2036. – reference: Chakrabarti A, Jha BK, Silverman RH. New insights into the role of RNase L in innate immunity. J Interferon Cytokine Res 2011; 31: 49-57. – reference: Dalakas MC. Pathogenesis and therapies of immune-mediated myopathies. Autoimmun Rev 2012; 11: 203-206. – reference: D'Cunha J, Knight E, Jr., Haas AL, et al. Immunoregulatory properties of ISG15, an interferon-induced cytokine. Proc Natl Acad Sci USA 1996; 93: 211-215. – reference: Greenberg SA, Sanoudou D, Haslett JN, et al. Molecular profiles of inflammatory myopathies. Neurology 2002; 59: 1170-1182. – reference: Larman HB, Salajegheh M, Nazareno R, et al. Cytosolic 5′-nucleotidase 1A autoimmunity in sporadic inclusion body myositis. Ann Neurol 2013; 73: 408-418. – reference: de Luna N, Gallardo E, Soriano M, et al. Absence of dysferlin alters myogenin expression and delays human muscle differentiation 'in vitro'. J Biol Chem 2006; 281: 17092-17098. – reference: Hornung V, Ellegast J, Kim S, et al. 5'-Triphosphate RNA is the ligand for RIG-I. Science 2006; 314: 994-997. – reference: Kuznik A, Bencina M, Svajger U, et al. Mechanism of endosomal TLR inhibition by antimalarial drugs and imidazoquinolines. J Immunol 2011; 186: 4794-4804. – reference: Castanier C, Garcin D, Vazquez A, et al. Mitochondrial dynamics regulate the RIG-I-like receptor antiviral pathway. EMBO Rep 2010; 11: 133-138. – reference: Casciola-Rosen L, Nagaraju K, Plotz P, et al. Enhanced autoantigen expression in regenerating muscle cells in idiopathic inflammatory myopathy. J Exp Med 2005; 201: 591-601. – reference: Mammen AL. Autoimmune myopathies: autoantibodies, phenotypes and pathogenesis. Nat Rev Neurol 2011; 7: 343-354. – reference: Nagaraju K, Casciola-Rosen L, Lundberg I, et al. Activation of the endoplasmic reticulum stress response in autoimmune myositis: potential role in muscle fiber damage and dysfunction. Arthritis Rheum 2005; 52: 1824-1835. – reference: Salajegheh M, Kong SW, Pinkus JL, et al. Interferon-stimulated gene 15 (ISG15) conjugates proteins in dermatomyositis muscle with perifascicular atrophy. Ann Neurol 2010; 67: 53-63. – reference: Yasukawa K, Oshiumi H, Takeda M, et al. Mitofusin 2 inhibits mitochondrial antiviral signaling. Sci Signal 2009; 2: ra47. – reference: Gallardo E, de Andres I, Illa I. Cathepsins are upregulated by IFN-γ/STAT1 in human muscle culture: a possible active factor in dermatomyositis. J Neuropathol Exp Neurol 2001; 60: 847-855. – reference: Tournadre A, Lenief V, Eljaafari A, et al. Immature muscle precursors are a source of interferon-β in myositis: role of Toll-like receptor 3 activation and contribution to HLA class I up-regulation. Arthritis Rheum 2012; 64: 533-541. – reference: De Luna N, Gallardo E, Sonnet C, et al. Role of thrombospondin 1 in macrophage inflammation in dysferlin myopathy. J Neuropathol Exp Neurol 2010; 69: 643-653. – reference: Kim GT, Cho ML, Park YE, et al. Expression of TLR2, TLR4, and TLR9 in dermatomyositis and polymyositis. Clin Rheumatol 2010; 29: 273-279. – reference: Dalakas MC, Hohlfeld R. Polymyositis and dermatomyositis. Lancet 2003; 362: 971-982. – reference: Poeck H, Bscheider M, Gross O, et al. Recognition of RNA virus by RIG-I results in activation of CARD9 and inflammasome signaling for interleukin 1β production. Nat Immunol 2010; 11: 63-69. – reference: Illa I, Gallardo E, Gimeno R, et al. Signal transducer and activator of transcription 1 in human muscle: implications in inflammatory myopathies. Am J Pathol 1997; 151: 81-88. – reference: Greenberg SA, Pinkus JL, Pinkus GS, et al. Interferon-α/β-mediated innate immune mechanisms in dermatomyositis. Ann Neurol 2005; 57: 664-678. – reference: Kawai T, Akira S. Toll-like receptor and RIG-I-like receptor signaling. Ann N Y Acad Sci 2008; 1143: 1-20. – reference: Smyth GK. Linear models and empirical bayes methods for assessing differential expression in microarray experiments. Stat Appl Genet Mol Biol 2004; 3: article 3. – reference: Hinson ER, Cresswell P. 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anti‐CADM‐140 antibody publication-title: Rheumatology (Oxford) – volume: 11: start-page: 203 year: 2012 end-page: 206 article-title: Pathogenesis and therapies of immune‐mediated myopathies publication-title: Autoimmun Rev – volume: 186: start-page: 4794 year: 2011 end-page: 4804 article-title: Mechanism of endosomal TLR inhibition by antimalarial drugs and imidazoquinolines publication-title: J Immunol – volume: 31: start-page: 3802 year: 2011 end-page: 3819 article-title: DDX60, a DEXD/H box helicase, is a novel antiviral factor promoting RIG‐I‐like receptor‐mediated signaling publication-title: Mol Cell Biol – volume: 52: start-page: 1824 year: 2005 end-page: 1835 article-title: Activation of the endoplasmic reticulum stress response in autoimmune myositis: potential role in muscle fiber damage and dysfunction publication-title: Arthritis Rheum – volume: 281: start-page: 17092 year: 2006 end-page: 17098 article-title: Absence of dysferlin alters myogenin expression and delays human muscle differentiation ' ' publication-title: J Biol Chem – volume: 67: start-page: 53 year: 2010 end-page: 63 article-title: Interferon‐stimulated gene 15 ( ) conjugates proteins in dermatomyositis muscle with perifascicular atrophy publication-title: Ann Neurol – volume: 7: start-page: 343 year: 2011 end-page: 354 article-title: Autoimmune myopathies: autoantibodies, phenotypes and pathogenesis publication-title: Nat Rev Neurol – volume: 73: start-page: 281 year: 2013 end-page: 293 article-title: Implication of double‐stranded RNA signaling in the etiology of autoimmune myasthenia gravis publication-title: Ann Neurol – volume: 69: start-page: 643 year: 2010 end-page: 653 article-title: Role of thrombospondin 1 in macrophage inflammation in dysferlin myopathy publication-title: J Neuropathol Exp Neurol – volume: 73: start-page: 408 year: 2013 end-page: 418 article-title: Cytosolic 5′‐nucleotidase 1A autoimmunity in sporadic inclusion body myositis publication-title: Ann Neurol – 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role of endogenous TLR ligands publication-title: J Pathol – volume: 64: start-page: 533 year: 2012 end-page: 541 article-title: Immature muscle precursors are a source of interferon‐ in myositis: role of Toll‐like receptor 3 activation and contribution to HLA class I up‐regulation publication-title: Arthritis Rheum – volume: 23: start-page: 19 year: 2005 end-page: 28 article-title: Cell type‐specific involvement of RIG‐I in antiviral response publication-title: Immunity – volume: 10: start-page: 534 year: 2011 end-page: 539 article-title: Viperin: a multifunctional, interferon‐inducible protein that regulates virus replication publication-title: Cell Host Microbe – volume: 448: start-page: 816 year: 2007 end-page: 819 article-title: Small self‐RNA generated by RNase L amplifies antiviral innate immunity publication-title: Nature – volume: 97: start-page: 9209 year: 2000 end-page: 9214 article-title: Conditional up‐regulation of MHC class I in skeletal muscle leads to self‐sustaining autoimmune myositis and myositis‐specific autoantibodies publication-title: Proc Natl Acad Sci USA – volume: 1: start-page: 167 year: 2011 end-page: 176 article-title: RIG‐I like receptors and their signaling crosstalk in the regulation of antiviral immunity publication-title: Curr Opin Virol – volume: 11: start-page: 63 year: 2010 end-page: 69 article-title: Recognition of RNA virus by RIG‐I results in activation of CARD9 and inflammasome signaling for interleukin 1 production publication-title: Nat Immunol – volume: 2 year: 2009 article-title: Mitofusin 2 inhibits mitochondrial antiviral signaling publication-title: Sci Signal – start-page: 1321 year: 2004 end-page: 1486 – volume: 76: start-page: 2079 year: 2011 end-page: 2088 article-title: Type I interferon and Toll‐like receptor expression characterizes inflammatory myopathies publication-title: Neurology – volume: 34: start-page: 680 year: 2011 end-page: 692 article-title: Immune signaling by RIG‐I‐like receptors 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| Snippet | We investigated the molecular mechanisms involved in the pathogenesis of three inflammatory myopathies, dermatomyositis (DM), polymyositis (PM) and inclusion... We investigated the molecular mechanisms involved in the pathogenesis of three inflammatory myopathies, dermatomyositis ( DM ), polymyositis ( PM ) and... |
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| SubjectTerms | Adult Aged Case-Control Studies Cells, Cultured DDX58 DEAD Box Protein 58 DEAD-box RNA Helicases - genetics DEAD-box RNA Helicases - metabolism dermatomyositis Dermatomyositis - genetics Dermatomyositis - immunology Dermatomyositis - metabolism Female Gene Expression Profiling - methods Gene Expression Regulation Genetic Association Studies Histocompatibility Antigens Class I - metabolism Humans Immunity, Innate Immunohistochemistry Inclusion Bodies - immunology Inclusion Bodies - metabolism inflammatory myopathy innate immunity Interferon-beta - metabolism Interferon-Induced Helicase, IFIH1 Male Microdissection Middle Aged Muscle Fibers, Skeletal - immunology Muscle Fibers, Skeletal - metabolism Oligonucleotide Array Sequence Analysis Polymyositis - genetics Polymyositis - immunology Polymyositis - metabolism Receptors, Immunologic RIG-I Signal Transduction Toll-Like Receptor 3 - genetics Toll-Like Receptor 3 - metabolism |
| Title | Altered RIG-I/DDX58-mediated innate immunity in dermatomyositis |
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