Amyloid deposits and inflammatory infiltrates in sporadic inclusion body myositis: the inflammatory egg comes before the degenerative chicken
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[1] J. Lünemann,et al. Beta-amyloid is a substrate of autophagy in sporadic inclusion body myositis. , 2007, Annals of neurology.
[2] Steven A Greenberg,et al. Evaluation and construction of diagnostic criteria for inclusion body myositis , 2014, Neurology.
[3] P H Plotz,et al. The Treatment of Inclusion Body Myositis: A Retrospective Review and a Randomized, Prospective Trial of Immunosuppressive , 1993, Medicine.
[4] A. Zwinderman,et al. Comparison of weakness progression in inclusion body myositis during treatment with methotrexate or placebo , 2002, Annals of neurology.
[5] K. Myburgh,et al. Variable inflammation and intramuscular STAT3 phosphorylation and myeloperoxidase levels after downhill running , 2014, Scandinavian journal of medicine & science in sports.
[6] D. Selkoe,et al. Twisted tubulofilaments of inclusion body myositis muscle resemble paired helical filaments of Alzheimer brain and contain hyperphosphorylated tau. , 1994, The American journal of pathology.
[7] S. Welle,et al. Ragged Red Fibers in Normal Aging and Inflammatory Myopathy , 1995, Annals of neurology.
[8] Anthony A Amato,et al. Unicorns, dragons, polymyositis, and other mythological beasts , 2003, Neurology.
[9] F. Breedveld,et al. Epidemiology of inclusion body myositis in the Netherlands: A nationwide study , 2000, Neurology.
[10] B. Engelen,et al. Autoantibodies to cytosolic 5′‐nucleotidase 1A in inclusion body myositis , 2013, Annals of neurology.
[11] M. Dalakas,et al. Interrelation of inflammation and APP in sIBM: IL-1β induces accumulation of β-amyloid in skeletal muscle , 2008, Brain : a journal of neurology.
[12] S. Spector,et al. A controlled study of intravenous immunoglobulin combined with prednisone in the treatment of IBM , 2001, Neurology.
[13] M. Sandri,et al. Proteotoxicity: an underappreciated pathology in cardiac disease. , 2014, Journal of molecular and cellular cardiology.
[14] V. Dubowitz,et al. INCREASED EXPRESSION OF HLA ABC CLASS I ANTIGENS BY MUSCLE FIBRES IN DUCHENNE MUSCULAR DYSTROPHY, INFLAMMATORY MYOPATHY, AND OTHER NEUROMUSCULAR DISORDERS , 1985, The Lancet.
[15] Clare Baecher-Allan,et al. Loss of Functional Suppression by CD4+CD25+ Regulatory T Cells in Patients with Multiple Sclerosis , 2004, The Journal of experimental medicine.
[16] I. James,et al. High-resolution HLA-DRB1 genotyping in an Australian inclusion body myositis (s-IBM) cohort: An analysis of disease-associated alleles and diplotypes , 2012, Journal of Neuroimmunology.
[17] E. Hoffman,et al. Activation of the endoplasmic reticulum stress response in autoimmune myositis: potential role in muscle fiber damage and dysfunction. , 2005, Arthritis and rheumatism.
[18] W. Engel,et al. Light and electron microscopic localization of beta-amyloid protein in muscle biopsies of patients with inclusion-body myositis. , 1992, The American journal of pathology.
[19] S. Greenberg. Inclusion body myositis: Review of recent literature , 2009, Current neurology and neuroscience reports.
[20] Steven A. Greenberg,et al. Autoantibodies against a 43 KDa Muscle Protein in Inclusion Body Myositis , 2011, PloS one.
[21] David Hilton-Jones,et al. Clinical assessment determines the diagnosis of inclusion body myositis independently of pathological features , 2013, Journal of Neurology, Neurosurgery & Psychiatry.
[22] Steven A Greenberg,et al. Sarcoplasmic redistribution of nuclear TDP‐43 in inclusion body myositis , 2009, Muscle & nerve.
[23] J. Kelly,et al. Secretion of amyloidogenic gelsolin progressively compromises protein homeostasis leading to the intracellular aggregation of proteins , 2009, Proceedings of the National Academy of Sciences.
[24] A. Broccolini,et al. TWEAK in inclusion-body myositis muscle: possible pathogenic role of a cytokine inhibiting myogenesis. , 2012, The American journal of pathology.
[25] K J Felice,et al. A pilot randomized trial of oxandrolone in inclusion body myositis , 2002, Neurology.
[26] J. Ju,et al. p97/VCP at the intersection of the autophagy and the ubiquitin proteasome system , 2010, Autophagy.
[27] A. Oldfors,et al. Anti–T-lymphocyte globulin treatment in inclusion body myositis , 2003, Neurology.
[28] R. Hohlfeld,et al. Coculture with autologous myotubes of cytotoxic T cells isolated from muscle in inflammatory myopathies , 1991, Annals of neurology.
[29] J. Piette,et al. CD4+CD25+ regulatory T-cell deficiency in patients with hepatitis C-mixed cryoglobulinemia vasculitis. , 2004, Blood.
[30] L. Servais,et al. Four-year longitudinal study of clinical and functional endpoints in sporadic inclusion body myositis: Implications for therapeutic trials , 2014, Neuromuscular Disorders.
[31] M. Dalakas. Polymyositis, dermatomyositis and inclusion-body myositis. , 1991, The New England journal of medicine.
[32] A. Pestronk,et al. Polymyositis: An overdiagnosed entity , 2004, Neurology.
[33] C. Loddenkemper,et al. Selective depletion of Foxp3+ regulatory T cells induces a scurfy-like disease , 2007, The Journal of experimental medicine.
[34] I. Targoff,et al. Novel Classification of Idiopathic Inflammatory Myopathies Based on Overlap Syndrome Features and Autoantibodies: Analysis of 100 French Canadian Patients , 2005, Medicine.
[35] I. Lundberg,et al. Expanded T cell receptor Vβ-restricted T cells from patients with sporadic inclusion body myositis are proinflammatory and cytotoxic CD28null T cells. , 2010, Arthritis and rheumatism.
[36] Pietro Fratta,et al. Proteasome inhibition and aggresome formation in sporadic inclusion-body myositis and in amyloid-beta precursor protein-overexpressing cultured human muscle fibers. , 2005, The American journal of pathology.
[37] M. Dalakas,et al. Inclusion body myositis: from immunopathology and degenerative mechanisms to treatment perspectives , 2013, Expert review of clinical immunology.
[38] B. De Paepe,et al. Role of cytokines and chemokines in idiopathic inflammatory myopathies , 2009, Current opinion in rheumatology.
[39] Andrew G Engel,et al. Correlation of muscle biopsy, clinical course, and outcome in PM and sporadic IBM , 2008, Neurology.
[40] I. Ferrer,et al. Expression of mutant ubiquitin (UBB+1) and p62 in myotilinopathies and desminopathies , 2007, Neuropathology and applied neurobiology.
[41] Randomized pilot trial of high-dose βINF-1a in patients with inclusion body myositis , 2004, Neurology.
[42] H. Ploegh,et al. Autoantibodies Produced at the Site of Tissue Damage Provide Evidence of Humoral Autoimmunity in Inclusion Body Myositis , 2012, PloS one.
[43] I. Nishino,et al. Allelic heterogeneity of GNE gene mutation in two Tunisian families with autosomal recessive inclusion body myopathy , 2005, Neuromuscular Disorders.
[44] M. Toepfer,et al. High-dose immunoglobulin therapy in sporadic inclusion body myositis: a double-blind, placebo-controlled study , 2000, Journal of Neurology.
[45] A. Berrebi,et al. Human monoclonal antibody derived from an autoimmune thrombocytopenic purpura patient, recognizing an intermediate filament's determinant common to vimentin and desmin. , 1990, Clinical immunology and immunopathology.
[46] C. Duyckaerts,et al. Th1 Response and Systemic Treg Deficiency in Inclusion Body Myositis , 2014, PloS one.
[47] I. James,et al. Frequency of autoantibodies and correlation with HLA-DRB1 genotype in sporadic inclusion body myositis (s-IBM): A population control study , 2012, Journal of Neuroimmunology.
[48] David Hilton-Jones,et al. Long-term observational study of sporadic inclusion body myositis. , 2011, Brain : a journal of neurology.
[49] Wolfgang Müller-Felber,et al. A novel homozygous missense mutation in the GNE gene of a patient with quadriceps-sparing hereditary inclusion body myopathy associated with muscle inflammation , 2003, Neuromuscular Disorders.
[50] J. Mendell,et al. Amyloid filaments in inclusion body myositis. Novel findings provide insight into nature of filaments. , 1991, Archives of neurology.
[51] W. Engel,et al. β-amyloid protein immunoreactivity in muscle of patients with inclusion-body myositis , 1992, The Lancet.
[52] R. Hohlfeld,et al. Inclusion Body Myositis , 2006, Neurology.
[53] M. Dalakas,et al. Provision of an explanation for the inefficacy of immunotherapy in sporadic inclusion body myositis: quantitative assessment of inflammation and β-amyloid in the muscle. , 2012, Arthritis and rheumatism.
[54] Olivier Boyer,et al. Shared blood and muscle CD8+ T-cell expansions in inclusion body myositis. , 2006, Brain : a journal of neurology.
[55] N. Lévy,et al. Translational Research and Therapeutic Perspectives in Dysferlinopathies , 2011, Molecular medicine.
[56] M. Sandri,et al. Misregulation of autophagy and protein degradation systems in myopathies and muscular dystrophies , 2013, Journal of Cell Science.
[57] G. Borm,et al. Diagnostic value of MHC class I staining in idiopathic inflammatory myopathies. , 2004, Journal of neurology, neurosurgery, and psychiatry.
[58] R. Gold,et al. Nitric oxide stress in sporadic inclusion body myositis muscle fibres: inhibition of inducible nitric oxide synthase prevents interleukin-1β-induced accumulation of β-amyloid and cell death. , 2012, Brain : a journal of neurology.
[59] J. Verschuuren,et al. A 12-year follow-up in sporadic inclusion body myositis: an end stage with major disabilities. , 2011, Brain : a journal of neurology.
[60] V. Askanas,et al. p62/SQSTM1 is overexpressed and prominently accumulated in inclusions of sporadic inclusion-body myositis muscle fibers, and can help differentiating it from polymyositis and dermatomyositis , 2009, Acta Neuropathologica.
[61] A. Engel,et al. Major histocompatibility complex class I antigen expression, immunolocalization of interferon subtypes, and T cell-mediated cytotoxicity in myopathies. , 1989, Human pathology.
[62] M. Dalakas,et al. Inclusion body myositis and myopathies , 1997, Journal of the Neurological Sciences.
[63] A. Engel,et al. Monoclonal antibody analysis of mononuclear cells in myopathies. I: Quantitation of subsets according to diagnosis and sites of accumulation and demonstration and counts of muscle fibers invaded by T cells , 1984, Annals of neurology.
[64] I. Nonaka,et al. Sialyllactose ameliorates myopathic phenotypes in symptomatic GNE myopathy model mice. , 2014, Brain : a journal of neurology.
[65] M. Dalakas,et al. Tragedy in a heartbeat: malfunctioning desmin causes skeletal and cardiac muscle disease. , 2009, The Journal of clinical investigation.
[66] J. Verschuuren,et al. Associations with autoimmune disorders and HLA class I and II antigens in inclusion body myositis , 2004, Neurology.
[67] M. Rose,et al. International Workshop : Inclusion Body Myositis , 2 – 4 December 2011 , Naarden , The Netherlands , 2013 .
[68] M. Dalakas,et al. Upregulated inducible co-stimulator (ICOS) and ICOS-ligand in inclusion body myositis muscle: significance for CD8+ T cell cytotoxicity. , 2004, Brain : a journal of neurology.
[69] R. Wada,et al. Conditional up-regulation of MHC class I in skeletal muscle leads to self-sustaining autoimmune myositis and myositis-specific autoantibodies. , 2000, Proceedings of the National Academy of Sciences of the United States of America.
[70] A. Pestronk,et al. TDP-43 accumulation in inclusion body myopathy muscle suggests a common pathogenic mechanism with frontotemporal dementia , 2008, Journal of Neurology, Neurosurgery, and Psychiatry.
[71] G. Pinkus,et al. Plasma cells in muscle in inclusion body myositis and polymyositis , 2005, Neurology.
[72] I. Nonaka,et al. Mutation profile of the GNE gene in Japanese patients with distal myopathy with rimmed vacuoles (GNE myopathy) , 2013, Journal of Neurology, Neurosurgery & Psychiatry.
[73] J. Rauch,et al. Hybridoma lupus autoantibodies can bind major cytoskeletal filaments in the absence of DNA-binding activity. , 1988, Arthritis and rheumatism.
[74] M. Dalakas,et al. HLA allele distribution distinguishes sporadic inclusion body myositis from hereditary inclusion body myopathies , 1998, Journal of Neuroimmunology.
[75] Frank M LaFerla,et al. Genetically augmenting Abeta42 levels in skeletal muscle exacerbates inclusion body myositis-like pathology and motor deficits in transgenic mice. , 2006, The American journal of pathology.
[76] Robert W. Taylor,et al. Mitochondrial and inflammatory changes in sporadic inclusion body myositis , 2015, Neuropathology and applied neurobiology.
[77] I. Nishino,et al. Cell stress molecules in the skeletal muscle of GNE myopathy , 2013, BMC Neurology.
[78] W. Engel,et al. Impaired autophagy in sporadic inclusion-body myositis and in endoplasmic reticulum stress-provoked cultured human muscle fibers. , 2010, The American journal of pathology.
[79] Olivier Boyer,et al. Long‐term persistence of clonally expanded T cells in patients with polymyositis , 2004, Annals of neurology.
[80] T. Maisonobe,et al. Diagnostic value of markers of muscle degeneration in sporadic inclusion body myositis , 2011, Acta myologica : myopathies and cardiomyopathies : official journal of the Mediterranean Society of Myology.
[81] Hanno Steen,et al. Cytosolic 5′‐nucleotidase 1A autoimmunity in sporadic inclusion body myositis , 2013, Annals of neurology.
[82] I. Nonaka,et al. Prophylactic treatment with sialic acid metabolites precludes the development of the myopathic phenotype in the DMRV-hIBM mouse model , 2009, Nature Medicine.
[83] W. Engel,et al. Sporadic inclusion-body myositis: A degenerative muscle disease associated with aging, impaired muscle protein homeostasis and abnormal mitophagy. , 2015, Biochimica et biophysica acta.
[84] H. Langen,et al. Antibody‐based proteomics and biomarker research—Current status and limitations , 2014, Proteomics.
[85] F. Heppner,et al. Luminescent Conjugated Oligothiophenes for Sensitive Fluorescent Assignment of Protein Inclusion Bodies , 2013, Chembiochem : a European journal of chemical biology.
[86] David Hilton-Jones,et al. A retrospective cohort study identifying the principal pathological features useful in the diagnosis of inclusion body myositis , 2014, BMJ Open.
[87] Marinos C. Dalakas,et al. β‐Amyloid is a substrate of autophagy in sporadic inclusion body myositis , 2007 .
[88] S. Kong,et al. Fast‐twitch sarcomeric and glycolytic enzyme protein loss in inclusion body myositis , 2009, Muscle & nerve.
[89] Lippincott Williams Wilkins,et al. Randomized pilot trial of βINF1a (Avonex) in patients with inclusion body myositis , 2002, Neurology.
[90] F. LaFerla,et al. Inflammation induces tau pathology in inclusion body myositis model via glycogen synthase kinase‐3β , 2008, Annals of neurology.
[91] J. Winkles,et al. TWEAK, a member of the TNF superfamily, is a multifunctional cytokine that binds the TweakR/Fn14 receptor. , 2003, Cytokine & growth factor reviews.
[92] W. Engel,et al. Sporadic inclusion-body myositis: conformational multifactorial ageing-related degenerative muscle disease associated with proteasomal and lysosomal inhibition, endoplasmic reticulum stress, and accumulation of amyloid-β42 oligomers and phosphorylated tau. , 2011, Presse medicale.
[93] W. F. Abdo,et al. Increased plasma amyloid-β42 protein in sporadic inclusion body myositis , 2009, Acta Neuropathologica.
[94] A. Pestronk. Acquired immune and inflammatory myopathies: pathologic classification , 2011, Current opinion in rheumatology.
[95] D. Piwnica-Worms,et al. Valosin-containing protein (VCP) is required for autophagy and is disrupted in VCP disease , 2009, The Journal of cell biology.
[96] David Hilton-Jones,et al. International Workshop on Inclusion Body Myositis held at the Institute of Myology, Paris, on 29 May 2009 , 2010, Neuromuscular Disorders.
[97] A. Filipovich,et al. Clinical and molecular features of the immunodysregulation, polyendocrinopathy, enteropathy, X linked (IPEX) syndrome , 2002, Journal of medical genetics.
[98] S. Greenberg. Comment on alemtuzumab and inclusion body myositis. , 2010, Brain : a journal of neurology.
[99] M. Dalakas,et al. Clonal restriction of T-cell receptor expression by infiltrating lymphocytes in inclusion body myositis persists over time. Studies in repeated muscle biopsies. , 2000, Brain : a journal of neurology.
[100] A. Goldberg,et al. Protein degradation and protection against misfolded or damaged proteins , 2003, Nature.
[101] W. Engel,et al. Dysferlin is a newly identified binding partner of AβPP and it co-aggregates with amyloid-β42 within sporadic inclusion-body myositis (s-IBM) muscle fibers , 2013, Acta Neuropathologica.
[102] M. Weller,et al. Human muscle cells express a B7‐related molecule, B7‐H1, with strong negative immune regulatory potential: a novel mechanism of counterbalancing the immune attack in idiopathic inflammatory myopathies , 2003, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
[103] Allan D. Kirk,et al. Effect of Alemtuzumab (CAMPATH 1-H) in patients with inclusion-body myositis , 2009, Brain : a journal of neurology.
[104] Friedell Gh. DRUGS IN HOSPITAL. , 1965 .
[105] F. Authier,et al. Overexpression of MHC class I in muscle of lymphocyte-deficient mice causes a severe myopathy with induction of the unfolded protein response. , 2013, The American journal of pathology.
[106] J. Dambrosia,et al. Treatment of inclusion-body myositis with IVIg , 1997, Neurology.
[107] A. Engel,et al. Sporadic inclusion body myositis: Counts of different types of abnormal fibers , 1996, Annals of neurology.