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COI: 1:CAS:528:DC%2BD2sXht1GgtbrP, PID: 17763431, This manuscript demonstrates a correlation between anti-Jo-1 antibody titers and parameters of muscular as well as extra-muscular disease activity
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Stone KB, Oddis CV, Fertig N, Katsumata Y, Lucas M, Vogt M, et al. Anti-Jo-1 antibody levels correlate with disease activity in idiopathic inflammatory myopathy. Arthritis Rheum. 2007;56:3125–31. This manuscript demonstrates a correlation between anti-Jo-1 antibody titers and parameters of muscular as well as extra-muscular disease activity.
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Yoshida S, Akizuki M, Mimori T, Yamagata H, Inada S, Homma M. The precipitating antibody to an acidic nuclear protein antigen, the Jo-1, in connective tissue diseases. A marker for a subset of polymyositis with interstitial pulmonary fibrosis. Arthritis Rheum. 1983;26:604–11.
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67650045885
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COI: 1:CAS:528:DC%2BD1MXptlKrsb4%3D, PID: 19565490
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17
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COI: 1:CAS:528:DC%2BD1MXotVCjtLY%3D, PID: 18628284
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Krystufkova O, Vallerskog T, Helmers SB, Mann H, Putova I, Belacek J, et al. Increased serum levels of B cell activating factor (BAFF) in subsets of patients with idiopathic inflammatory myopathies. Ann Rheum Dis. 2009;68:836–43.
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18
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68049108408
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Barbasso Helmers S, Englund P, Engstrom M, Ahlin E, Fathi M, Janciauskiene S, et al. Sera from anti-Jo-1-positive patients with polymyositis and interstitial lung disease induce expression of intercellular adhesion molecule 1 in human lung endothelial cells. Arthritis Rheum. 2009;60:2524–30.
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19
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Critical requirement for professional APCs in eliciting T cell responses to novel fragments of histidyl-tRNA synthetase (Jo-1) in Jo-1 antibody-positive polymyositis
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COI: 1:CAS:528:DC%2BD38XpsFGjtro%3D, PID: 12471150
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Ascherman DP, Oriss TB, Oddis CV, Wright TM. Critical requirement for professional APCs in eliciting T cell responses to novel fragments of histidyl-tRNA synthetase (Jo-1) in Jo-1 antibody-positive polymyositis. J Immunol. 2002;169:7127–34.
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20
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0030819072
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Myositis induced by naked DNA immunization with the gene for histidyl-tRNA synthetase
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COI: 1:CAS:528:DyaK2sXlsFGjsbk%3D, PID: 9287147, This work shows that intramuscular immunization with a cDNA construct expressing human histidyl-tRNA synthetase induces low level anti-Jo-1 antibody responses as well as localized muscle inflammation; at the same time, these studies highlight some of the key variables distinguishing immune responses to protein/adjuvant combinations from those triggered by DNA immunization
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Blechynden LM, Lawson MA, Tabarias H, Garlepp MJ, Sherman J, Raben N, et al. Myositis induced by naked DNA immunization with the gene for histidyl-tRNA synthetase. Hum Gene Ther. 1997;8:1469–80. This work shows that intramuscular immunization with a cDNA construct expressing human histidyl-tRNA synthetase induces low level anti-Jo-1 antibody responses as well as localized muscle inflammation; at the same time, these studies highlight some of the key variables distinguishing immune responses to protein/adjuvant combinations from those triggered by DNA immunization.
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Blechynden, L.M.1
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21
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34548594045
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Species-specific immune responses generated by histidyl-tRNA synthetase immunization are associated with muscle and lung inflammation
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COI: 1:CAS:528:DC%2BD2sXhtVCmur3K, PID: 17826948, Based on an antigen/adjuvant immunization strategy, this work illustrates the importance of species-specific immune responses against HRS in determining phenotypic expression of myositis as well as inflammatory lung disease characteristic of the anti-synthetase syndrome
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Katsumata Y, Ridgway WM, Oriss T, Gu X, Chin D, Wu Y, et al. Species-specific immune responses generated by histidyl-tRNA synthetase immunization are associated with muscle and lung inflammation. J Autoimmun. 2007;29:174–86. Based on an antigen/adjuvant immunization strategy, this work illustrates the importance of species-specific immune responses against HRS in determining phenotypic expression of myositis as well as inflammatory lung disease characteristic of the anti-synthetase syndrome.
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J Autoimmun
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Katsumata, Y.1
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Wu, Y.6
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22
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0033515887
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Two distinct cytokines released from a human aminoacyl-tRNA synthetase
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COI: 1:CAS:528:DyaK1MXitlCnu7c%3D, PID: 10102815, This paradigm-shifting work demonstrated that tyrosyl-tRNA synthetase possesses non-enzymatic, cytokine-like properties
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Wakasugi K, Schimmel P. Two distinct cytokines released from a human aminoacyl-tRNA synthetase. Science. 1999;284:147–51. This paradigm-shifting work demonstrated that tyrosyl-tRNA synthetase possesses non-enzymatic, cytokine-like properties.
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Wakasugi, K.1
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Histidyl-tRNA synthetase and asparaginyl-tRNA synthetase, autoantigens in myositis, activate chemokine receptors on T lymphocytes and immature dendritic cells
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COI: 1:CAS:528:DC%2BD38Xnt1yhtL4%3D, PID: 12235211, Consistent with previous observations pertaining to tyrosyl-tRNA synthetase, these studies detail chemokine-like properties of two additional tRNA synthetases targeted in the anti-synthetase syndrome—histidyl-tRNA synthetase (HRS = Jo-1) and asparaginyl-tRNA synthetase (ARS = KS)
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Howard OM, Dong HF, Yang D, Raben N, Nagaraju K, Rosen A, et al. Histidyl-tRNA synthetase and asparaginyl-tRNA synthetase, autoantigens in myositis, activate chemokine receptors on T lymphocytes and immature dendritic cells. J Exp Med. 2002;196:781–91. Consistent with previous observations pertaining to tyrosyl-tRNA synthetase, these studies detail chemokine-like properties of two additional tRNA synthetases targeted in the anti-synthetase syndrome—histidyl-tRNA synthetase (HRS = Jo-1) and asparaginyl-tRNA synthetase (ARS = KS).
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J Exp Med
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Howard, O.M.1
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24
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84904209763
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Secreted histidyl-tRNA synthetase splice variants elaborate major epitopes for autoantibodies in inflammatory myositis
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COI: 1:CAS:528:DC%2BC2cXhtFCktLzK, PID: 24898250
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Zhou JJ, Wang F, Xu Z, Lo WS, Lau CF, Chiang KP, et al. Secreted histidyl-tRNA synthetase splice variants elaborate major epitopes for autoantibodies in inflammatory myositis. J Biol Chem. 2014;289:19269–75.
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25
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84904240920
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Enhanced formation and impaired degradation of neutrophil extracellular traps in dermatomyositis and polymyositis: a potential contributor to interstitial lung disease complications
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COI: 1:CAS:528:DC%2BC2cXps1Kku7g%3D, PID: 24611519
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Zhang S, Shu X, Tian X, Chen F, Lu X, Wang G. Enhanced formation and impaired degradation of neutrophil extracellular traps in dermatomyositis and polymyositis: a potential contributor to interstitial lung disease complications. Clin Exp Immunol. 2014;177:134–41.
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26
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34848898509
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A possible mechanism for endogenous activation of the type I interferon system in myositis patients with anti-Jo-1 or anti-Ro 52/anti-Ro 60 autoantibodies
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COI: 1:CAS:528:DC%2BD2sXht1GgtbrO, PID: 17763410, These in vitro studies provide a plausible mechanism linking Jo-1/anti-Jo-1 immune complex formation to activation of endosomal toll-like receptors and subsequent elaboration of Type I interferons involved in innate immune signaling pathways
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Eloranta ML, Barbasso Helmers S, Ulfgren AK, Ronnblom L, Alm GV, Lundberg IE. A possible mechanism for endogenous activation of the type I interferon system in myositis patients with anti-Jo-1 or anti-Ro 52/anti-Ro 60 autoantibodies. Arthritis Rheum. 2007;56:3112–24. These in vitro studies provide a plausible mechanism linking Jo-1/anti-Jo-1 immune complex formation to activation of endosomal toll-like receptors and subsequent elaboration of Type I interferons involved in innate immune signaling pathways.
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Arthritis Rheum
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Eloranta, M.L.1
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Lundberg, I.E.6
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27
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84923605605
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Required role of apoptotic myogenic precursors and toll-like receptor stimulation for the establishment of autoimmune myositis in experimental murine models
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COI: 1:CAS:528:DC%2BC2MXjtlSlsLs%3D, PID: 25504878
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Sciorati C, Monno A, Ascherman DP, Seletti E, Manfredi AA, Rovere-Querini P. Required role of apoptotic myogenic precursors and toll-like receptor stimulation for the establishment of autoimmune myositis in experimental murine models. Arthritis Rheumatol. 2015;67:809–22.
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28
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79551668080
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Role of innate immunity in a murine model of histidyl-transfer RNA synthetase (Jo-1)-mediated myositis
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COI: 1:CAS:528:DC%2BC3MXivVOksrk%3D, PID: 21280002, This manuscript details the development of an alternative, antigen (HRS)-induced model of myositis (based on intramuscular immunization with recombinant HRS in the absence of additional exogenous adjuvant) that features HRS-mediated activation of innate immune responses
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Soejima M, Kang EH, Gu X, Katsumata Y, Clemens PR, Ascherman DP. Role of innate immunity in a murine model of histidyl-transfer RNA synthetase (Jo-1)-mediated myositis. Arthritis Rheum. 2011;63:479–87. This manuscript details the development of an alternative, antigen (HRS)-induced model of myositis (based on intramuscular immunization with recombinant HRS in the absence of additional exogenous adjuvant) that features HRS-mediated activation of innate immune responses.
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Arthritis Rheum
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29
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84881437334
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Functional redundancy of MyD88-dependent signaling pathways in a murine model of histidyl-transfer RNA synthetase-induced myositis
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COI: 1:CAS:528:DC%2BC3sXht1WitbrN, PID: 23842751, As a follow up to reference 28, this work defines the central role of MyD88-dependent signaling pathways in the intramuscular immunization model of HRS-induced myositis and highlights the unique capacity of HRS to interact with various endogenous/exogenous ligands of MyD88-dependent toll-like receptors
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Fernandez I, Harlow L, Zang Y, Liu-Bryan R, Ridgway WM, Clemens PR, et al. Functional redundancy of MyD88-dependent signaling pathways in a murine model of histidyl-transfer RNA synthetase-induced myositis. J Immunol. 2013;191:1865–72. As a follow up to reference 28, this work defines the central role of MyD88-dependent signaling pathways in the intramuscular immunization model of HRS-induced myositis and highlights the unique capacity of HRS to interact with various endogenous/exogenous ligands of MyD88-dependent toll-like receptors.
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J Immunol
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Fernandez, I.1
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30
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Effects of HMGB1 on in vitro responses of isolated muscle fibers and functional aspects in skeletal muscles of idiopathic inflammatory myopathies
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COI: 1:CAS:528:DC%2BC3cXhs1Ggsrw%3D, PID: 19837864
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31
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84880132910
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TLR4 as receptor for HMGB1 induced muscle dysfunction in myositis
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Zong M, Bruton JD, Grundtman C, Yang H, Li JH, Alexanderson H, Palmblad K, Andersson U, Harris HE, Lundberg IE, et al.: TLR4 as receptor for HMGB1 induced muscle dysfunction in myositis. Ann Rheum Dis 2012.
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Ann Rheum Dis
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Zong, M.1
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Toll-like receptors promote inflammation in idiopathic inflammatory myopathies
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COI: 1:CAS:528:DC%2BC38XhsVWntLjP, PID: 22964787, This analysis provides compelling evidence that TLR-mediated signaling pathways are operative in muscle tissue derived from myositis patients
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Brunn A, Zornbach K, Hans VH, Haupt WF, Deckert M. Toll-like receptors promote inflammation in idiopathic inflammatory myopathies. J Neuropathol Exp Neurol. 2012;71:855–67. This analysis provides compelling evidence that TLR-mediated signaling pathways are operative in muscle tissue derived from myositis patients.
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