From Diagnosis to Prognosis: Revisiting the Meaning of Muscle ISG15 Overexpression in Juvenile Inflammatory Myopathies.


Journal

Arthritis & rheumatology (Hoboken, N.J.)
ISSN: 2326-5205
Titre abrégé: Arthritis Rheumatol
Pays: United States
ID NLM: 101623795

Informations de publication

Date de publication:
06 2021
Historique:
revised: 24 11 2020
received: 20 05 2020
accepted: 10 12 2020
pubmed: 15 12 2020
medline: 13 8 2021
entrez: 14 12 2020
Statut: ppublish

Résumé

Juvenile idiopathic inflammatory/immune myopathies (IIMs) constitute a highly heterogeneous group of disorders with diagnostic difficulties and prognostic uncertainties. Circulating myositis-specific autoantibodies (MSAs) have been recognized as reliable tools for patient substratification. Considering the key role of type I interferon (IFN) up-regulation in juvenile IIM, we undertook the present study to investigate whether IFN-induced 15-kd protein (ISG-15) could be a reliable biomarker for stratification and diagnosis and to better elucidate its role in juvenile IIM pathophysiology. The study included 56 patients: 24 with juvenile dermatomyositis (DM), 12 with juvenile overlap myositis (OM), 10 with Duchenne muscular dystrophy, and 10 with congenital myopathies. Muscle biopsy samples were assessed by immunohistochemistry, immunoblotting, and real-time quantitative polymerase chain reaction. Negative regulators of type I IFN (ISG15 and USP18) and positive regulators of type I IFN (DDX58 and IFIH1) were analyzed. ISG15 expression discriminated patients with juvenile IIM from those with nonimmune myopathies and, among patients with juvenile IIM, discriminated those with DM from those with OM. Among patients with juvenile DM, up-regulation of the type I IFN positive regulators DDX58 and IFIH1 was similar regardless of MSA status. In contrast, the highest levels of the type I IFN negative regulator ISG15 were observed in patients who were positive for melanoma differentiation-associated gene 5 (MDA-5). Finally, ISG15 levels were inversely correlated with the severity of muscle histologic abnormalities and positively correlated with motor performance as evaluated by the Childhood Myositis Assessment Scale and by manual muscle strength testing. Muscle ISG15 expression is strongly associated with juvenile DM, with patients exhibiting a different ISG-15 muscle signature according to their MSA class. Patients with juvenile DM who are positive for MDA-5 have higher expression of ISG15 in both gene form and protein form compared to the other subgroups. Moreover, our data show that negative regulation of type I IFN correlates with milder muscle involvement.

Identifiants

pubmed: 33314705
doi: 10.1002/art.41625
doi:

Substances chimiques

Autoantibodies 0
Biomarkers 0
Cytokines 0
Receptors, Immunologic 0
Ubiquitins 0
ISG15 protein, human 60267-61-0
USP18 protein, human EC 3.4.19.12
Ubiquitin Thiolesterase EC 3.4.19.12
RIGI protein, human EC 3.6.1.-
IFIH1 protein, human EC 3.6.1.-
DEAD Box Protein 58 EC 3.6.4.13
Interferon-Induced Helicase, IFIH1 EC 3.6.4.13

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1044-1052

Commentaires et corrections

Type : CommentIn
Type : CommentIn

Informations de copyright

© 2020, American College of Rheumatology.

Références

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Auteurs

Cyrielle Hou (C)

Institut Mondor de Recherche Biomédicale, Université Paris-Est Créteil, INSERM, Paris, France.

Chloé Durrleman (C)

Institut Mondor de Recherche Biomédicale, Université Paris-Est Créteil, INSERM, Centre de Reference pour les Maladies Neuromusculaires, FILNEMUS, Paris, France.

Baptiste Periou (B)

Institut Mondor de Recherche Biomédicale, Université Paris-Est Créteil, INSERM, Hôpital Henri-Mondor, AP-HP, Paris, France.

Christine Barnerias (C)

Centre de Reference pour les Maladies Neuromusculaires, FILNEMUS, Paris, France.

Christine Bodemer (C)

Hôpital Necker-Enfants Malades, AP-HP, Paris, France.

Isabelle Desguerre (I)

Centre de Reference pour les Maladies Neuromusculaires, FILNEMUS, Paris, France.

Pierre Quartier (P)

Hôpital Necker-Enfants Malades, AP-HP, Paris, France.

Isabelle Melki (I)

Laboratoire de Neurogénétique et Neuroinflammation, Institut Imagine, Hôpital Necker-Enfants Malades, AP-HP, Paris, France.

Gillian I Rice (GI)

University of Manchester School of Biological Sciences, Manchester, UK.

Mathieu P Rodero (MP)

Laboratoire de Chimie et Biologie, Modélisation et Immunologie pour la Thérapie, CNRS UMR 8601, Université Paris-Descartes, Paris, France.

Jean-Luc Charuel (JL)

Hôpital Pitié-Salpêtrière, AP-HP, Paris, France.

Fréderic Relaix (F)

Institut Mondor de Recherche Biomédicale, Université Paris-Est Créteil, INSERM, Paris, France.

Brigitte Bader-Meunier (B)

Hôpital Necker-Enfants Malades, AP-HP, Paris, France.

FrançoisJérôme Authier (F)

Institut Mondor de Recherche Biomédicale, Université Paris-Est Créteil, INSERM, Centre de Reference pour les Maladies Neuromusculaires, Hôpital Henri-Mondor, AP-HP, FILNEMUS, Paris, France.

Cyril Gitiaux (C)

Institut Mondor de Recherche Biomédicale, Université Paris-Est Créteil, INSERM, Centre de Reference pour les Maladies Neuromusculaires, Hôpital Necker-Enfants Malades, AP-HP, FILNEMUS, Paris, France.

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