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Articles by Werner Stenzel
CD19 CAR T cell therapy for treatment-refractory seropositive rheumatoid arthritis: a phase 1 trial
Abstract Chimeric antigen receptor (CAR) T cell-mediated B cell depletion has demonstrated efficacy in several autoimmune diseases. Here we report clinical and molecular data obtained during the nonrandomized phase 1 part of the phase 1/2 COMPARE trial, evaluating safety and efficacy of mivocabtagene autoleucel (miv-cel), an autologous fully human CD19 CAR T cell therapy, in rheumatoid arthritis (RA).
Inflammation reprograms fibro-adipogenic progenitors to sustain immunopathogenic niches in myositis
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Abstract Idiopathic inflammatory myopathies (IIMs) are autoimmune disorders defined by persistent muscle inflammation, fibrosis, and frequent resistance to current therapies. However, the mechanisms perpetuating disease activity despite immunosuppressive treatment remain elusive. Here, we describe a novel role for tissue-resident stromal cells, specifically fibro-adipogenic progenitors (FAPs), in sustaining skeletal muscle inflammation.
By Christopher Nelke, Jin-Soo Park, Christina B. Schroeter, Felix Kleefeld, Anne-Katrin Güttsches, Sara Walli, Corinna Preusse, Alexander Mensch, Anne Schänzer, Markus Leo, Tim Hagenacker, Benedikt Schoser, Jörg H. W. Distler, Akiyoshi Uezumi, Werner Stenzel, Sven G. Meuth, Olivier Benveniste, Yves Allenbach, Tobias Ruck, Julian Sanchez-Dal Cin, Charles-Antoine Dallevet, Jacqueline C. Kinold, Paula Quint, Derya Cengiz, Vera Dobelmann
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Nature
Verified
Volume 148 Issue 8
Interferon-γ causes myogenic cell dysfunction and senescence in immune myopathies Immune myopathies are disabling acquired diseases that can be resistant to immunosuppressive treatment. Hou et al. show that interferon-gamma impairs muscle regeneration, and that the JAK1/2 inhibitor ruxolitinib can counteract this effect, suggesting that it may offer a new therapeutic option for refractory myositis. See Stenzel et al.
More than meets the eye
Autoantibodies Autoimmunity Granulomatosis with polyangiitis Rituximab Vasculitis A 28-year-old man presented with a 4-month history of a prednisolone-sensitive, painful and progressive right-sided exophthalmos and consecutive diplopia.
Reader Response: Clinical Subgroups and Factors Associated With Progression in Patients With Inclusion Body Myositis
We read with interest the article by Michelle et al.1 about clinical subgroups and factors associated with progression in patients with inclusion body myositis (IBM). The authors used Griggs criteria,2 European Neuromuscular Centre 2011 criteria, and Lloyd Greenberg data-derived criteria,3 including endomysial inflammation, invasion of non-necrotic fibers, and rimmed vacuoles. Footnotes Author disclosures are available upon request (journal{at}neurology.org). See Editors' Note See response
Whole-Genome Sequencing Identified New Structural Variations in the DMD Gene That Cause Duchenne Muscular Dystrophy in Two Girls
1. Introduction Duchenne muscular dystrophy (DMD, MIM #310200) is the most frequent inherited muscle disorder caused by truncating mutations, mainly frameshift deletions or nonsense variants, in the huge DMD gene located on Xp21.2-p21.1 (MIM *300377).
Unconvincing Evidence of SARS-CoV-2-Associated Myositis in Autopsied Muscles-Reply
Comment & Response November 22, 2021 JAMA Neurol. Published online November 22, 2021.
Immune-mediated necrotizing myopathy: clinical features and pathogenesis
Abstract Immune-mediated necrotizing myopathy (IMNM) is a group of inflammatory myopathies that was distinguished from polymyositis in 2004. Most IMNMs are associated with anti-signal recognition particle (anti-SRP) or anti-3-hydroxy-3-methylglutaryl-coA reductase (anti-HMGCR) myositis-specific autoantibodies, although ~20% of patients with IMNM remain seronegative. These associations have led to three subclasses of IMNM: anti-SRP-positive IMNM, anti-HMGCR-positive IMNM and seronegative IMNM.
Aicardi-Goutières-Syndrome with muscle involvement in early infancy
Aicardi-Goutières-syndrome (AGS) comprises a group of monogenetic disorders characterized by aberrant immune activation (1). The spectrum of neurological features includes acquired microcephaly with cerebral atrophy, basal ganglia calcification, leukodystrophy, chronic cerebrospinal lymphocytosis, and/or elevated concentration of type I interferons (IFNs) resulting in high morbidity and mortality (2). AGS can be caused by mutations in several genes involved in sensing or modifying nucleic acids.
Neuropathology and Applied Neurobiology
EditorialRecent advances in MyopathologyAuthorsWerner Stenzel,Department of Neuropathology, Berlin, GermanySearch for more papers by this authorHans-Hilmar GoebelDepartment of Neuropathology, Berlin, GermanySearch for more papers by this authorNo abstract is available for this article.AncillaryArticle InformationFormat AvailableFull text: HTML | PDF© 2017 British Neuropathological Society Request Permissions Publication HistoryIssue online: 15 March 2017Version of record online: 15 March...
MORC2 mutation causes severe spinal muscular atrophy-phenotype, cerebellar atrophy, and diaphragmatic paralysis
Sir,With great interest, we read the article by Sevilla et al. (2016) delineating mutations in MORC2 as a novel genetic cause for axonal Charcot-Marie-Tooth (CMT) disease type 2Z (OMIM #616688) with dominant inheritance. The authors detected MORC2 mutations in nine patients from three unrelated families and showed MORC2 to be expressed in both axons and Schwann cells of the peripheral nerve (Sevilla et al., 2016).
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