SIGLEC1 enables straightforward assessment of type I interferon activity in idiopathic inflammatory myopathies.


Journal

RMD open
ISSN: 2056-5933
Titre abrégé: RMD Open
Pays: England
ID NLM: 101662038

Informations de publication

Date de publication:
02 2022
Historique:
received: 13 09 2021
accepted: 23 01 2022
entrez: 18 2 2022
pubmed: 19 2 2022
medline: 7 4 2022
Statut: ppublish

Résumé

To evaluate sialic acid binding Ig-like lectin 1 (SIGLEC1) expression on monocytes by flow cytometry as a type I interferon biomarker in idiopathic inflammatory myopathies (IIM). We performed a retrospective analysis of adult and paediatric patients with the diagnosis of IIM. SIGLEC1 expression was assessed by flow cytometry and was compared with Physician Global Assessment or Childhood Myositis Assessment Scale disease activity scores. Mann Whitney U test and receiver operating characteristic curves were used for cross-sectional data analysis (n=96), two-level mixed-effects linear regression model for longitudinal analyses (n=26, 110 visits). Response to treatment was analysed in 14 patients within 12 months, using Wilcoxon test. SIGLEC1 was compared with interferon-stimulated gene 15/MxA status by immunohistochemical staining of muscle biopsies (n=17). 96 patients with adult (a) and juvenile (j) dermatomyositis (DM, n=38), antisynthetase syndrome (AS, n=19), immune-mediated necrotising myopathy (IMNM, n=8), inclusion body myositis (IBM, n=9) and overlap myositis (n=22) were included. SIGLEC1 distinguished significantly between active and inactive disease with an area under the curve of 0.92 (95% CI 0.83 to 1) in DM and correlated with disease activity longitudinally (aDM: standardised beta=0.54, p<0.001; jDM: standardised beta=-0.70, p<0.001). Response to treatment in DM was associated with a decreasing SIGLEC1 (p<0.01, Wilcoxon test). SIGLEC1 was found upregulated in 8 of 19 patients with AS, 2 of 9 patients with IBM but not in IMNM. SIGLEC1 is a candidate biomarker to assess type I interferon activity in IIM and proved useful for monitoring disease activity and response to treatment in juvenile and adult DM.

Identifiants

pubmed: 35177553
pii: rmdopen-2021-001934
doi: 10.1136/rmdopen-2021-001934
pmc: PMC8860073
pii:
doi:

Substances chimiques

Interferon Type I 0
SIGLEC1 protein, human 0
Sialic Acid Binding Ig-like Lectin 1 0

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

© Author(s) (or their employer(s)) 2022. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.

Déclaration de conflit d'intérêts

Competing interests: None declared.

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Auteurs

Manuel Graf (M)

Department of Rheumatology and Clinical Immunology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.

Sae Lim von Stuckrad (SL)

Department of Pediatric Pneumology, Immunology and Critical Care Medicine and SPZ (Center for Chronically Sick Children), Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.

Akinori Uruha (A)

Department of Neuropathology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.
Department of Neurology, Tokyo Metropolitan Neurological Hospital, Fuchu, Tokyo, Japan.

Jens Klotsche (J)

German Rheumatism Research Center Berlin - a Leibniz Institute (DRFZ), Berlin, Germany.

Lydia Zorn-Pauly (L)

Department of Rheumatology and Clinical Immunology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.

Nadine Unterwalder (N)

Department of Immunology, Labor Berlin - Charité Vivantes GmbH, Berlin, Germany.

Thomas Buttgereit (T)

Department of Dermatology and Allergy, Dermatological Allergology, Allergie-Centrum-Charité, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.

Martin Krusche (M)

Department of Rheumatology and Clinical Immunology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.

Christian Meisel (C)

Department of Immunology, Labor Berlin - Charité Vivantes GmbH, Berlin, Germany.

Gerd R Burmester (GR)

Department of Rheumatology and Clinical Immunology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.

Falk Hiepe (F)

Department of Rheumatology and Clinical Immunology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.

Robert Biesen (R)

Department of Rheumatology and Clinical Immunology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.

Tilmann Kallinich (T)

Department of Pediatric Pneumology, Immunology and Critical Care Medicine and SPZ (Center for Chronically Sick Children), Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.
German Rheumatism Research Center Berlin - a Leibniz Institute (DRFZ), Berlin, Germany.

Werner Stenzel (W)

Department of Neuropathology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.

Udo Schneider (U)

Department of Rheumatology and Clinical Immunology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.

Thomas Rose (T)

Department of Rheumatology and Clinical Immunology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany thomas.rose@charite.de.

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