Identification of connective tissue disease autoantibodies and a novel autoantibody anti-annexin A11 in patients with "idiopathic" interstitial lung disease.

Autoantibody Connective tissue disease Diagnostic assay Interstitial lung disease Myositis Systemic sclerosis

Journal

Clinical immunology (Orlando, Fla.)
ISSN: 1521-7035
Titre abrégé: Clin Immunol
Pays: United States
ID NLM: 100883537

Informations de publication

Date de publication:
02 Apr 2024
Historique:
received: 17 01 2024
revised: 07 03 2024
accepted: 01 04 2024
medline: 5 4 2024
pubmed: 5 4 2024
entrez: 4 4 2024
Statut: aheadofprint

Résumé

Autoantibodies are a hallmark feature of Connective Tissue Diseases (CTD). Their presence in patients with idiopathic interstitial lung disease (ILD) may suggest covert CTD. We aimed to determine the prevalence of CTD autoantibodies in patients diagnosed with idiopathic ILD. 499 patient sera were analysed: 251 idiopathic pulmonary fibrosis (IPF), 206 idiopathic non-specific interstitial pneumonia (iNSIP) and 42 cryptogenic organising pneumonia (COP). Autoantibody status was determined by immunoprecipitation. 2.4% of IPF sera had a CTD-autoantibody compared to 10.2% of iNSIP and 7.3% of COP. 45% of autoantibodies were anti-synthetases. A novel autoantibody targeting an unknown 56 kDa protein was found in seven IPF patients (2.8%) and two NSIP (1%) patients. This was characterised as anti-annexin A11. Specific guidance on autoantibody testing and interpretation in patients with ILD could improve diagnostic accuracy. Further work is required to determine the clinical significance of anti-annexin A11.

Sections du résumé

BACKGROUND BACKGROUND
Autoantibodies are a hallmark feature of Connective Tissue Diseases (CTD). Their presence in patients with idiopathic interstitial lung disease (ILD) may suggest covert CTD. We aimed to determine the prevalence of CTD autoantibodies in patients diagnosed with idiopathic ILD.
METHODS METHODS
499 patient sera were analysed: 251 idiopathic pulmonary fibrosis (IPF), 206 idiopathic non-specific interstitial pneumonia (iNSIP) and 42 cryptogenic organising pneumonia (COP). Autoantibody status was determined by immunoprecipitation.
RESULTS RESULTS
2.4% of IPF sera had a CTD-autoantibody compared to 10.2% of iNSIP and 7.3% of COP. 45% of autoantibodies were anti-synthetases. A novel autoantibody targeting an unknown 56 kDa protein was found in seven IPF patients (2.8%) and two NSIP (1%) patients. This was characterised as anti-annexin A11.
CONCLUSION CONCLUSIONS
Specific guidance on autoantibody testing and interpretation in patients with ILD could improve diagnostic accuracy. Further work is required to determine the clinical significance of anti-annexin A11.

Identifiants

pubmed: 38575043
pii: S1521-6616(24)00092-5
doi: 10.1016/j.clim.2024.110201
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

110201

Informations de copyright

Copyright © 2024. Published by Elsevier Inc.

Déclaration de conflit d'intérêts

Declaration of competing interest The authors have no conflicts of interest to declare.

Auteurs

Sarah L Tansley (SL)

Department of Life Sciences, University of Bath, Bath, UK; Royal National Hospital for Rheumatic Diseases, Bath, UK; Kings College Hospital NHS Foundation Trust, London, UK; Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield, UK. Electronic address: slt32@bath.ac.uk.

Fionnuala McMorrow (F)

Department of Life Sciences, University of Bath, Bath, UK.

Caroline V Cotton (CV)

Liverpool University Hospitals NHS Trust, Liverpool, UK.

Huzaifa Adamali (H)

Bristol Interstitial Lung Disease service, North Bristol NHS Trust, Bristol, UK.

Shaney L Barratt (SL)

Bristol Interstitial Lung Disease service, North Bristol NHS Trust, Bristol, UK.

Zoe E Betteridge (ZE)

Department of Life Sciences, University of Bath, Bath, UK.

Janire Perurena-Prieto (J)

Vall d'Hebron University Hospital (HUVH), Barcelona, Spain.

Michael A Gibbons (MA)

College of Medicine & Health, University of Exeter; Royal Devon University Hospitals Foundation NHS Trust.

Raman Kular (R)

Royal Devon University Hospitals Foundation NHS Trust.

Aravinthan Loganathan (A)

Department of Life Sciences, University of Bath, Bath, UK; Royal National Hospital for Rheumatic Diseases, Bath, UK.

Janine A Lamb (JA)

Faculty of Biology, Medicine and Health, University of Manchester, UK.

Hui Lu (H)

Department of Life Sciences, University of Bath, Bath, UK.

Robert P New (RP)

Division of Musculoskeletal and dermatological Sciences, University of Manchester, UK.

Diane Pratt (D)

Bristol Interstitial Lung Disease service, North Bristol NHS Trust, Bristol, UK.

Pilar Rivera-Ortega (P)

Manchester University NHS Foundation Trust, Manchester, UK.

Ross Sayers (R)

College of Medicine & Health, University of Exeter.

Matthew Steward (M)

College of Medicine & Health, University of Exeter.

Lachlan Stranks (L)

Manchester University NHS Foundation Trust, Manchester, UK.

Edward Vital (E)

Leeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds, Leeds, UK; NIHR Leeds Biomedical Research Centre, Leeds Teaching Hospitals NHS Trust, Leeds, UK.

Lisa G Spencer (LG)

Liverpool Interstitial Lung Disease Service, Aintree Hospital, Liverpool University Hospitals NHS Foundation Trust, Liverpool, UK.

Neil J McHugh (NJ)

Department of Life Sciences, University of Bath, Bath, UK.

Robert G Cooper (RG)

Liverpool Interstitial Lung Disease Service, Aintree Hospital, Liverpool University Hospitals NHS Foundation Trust, Liverpool, UK.

Classifications MeSH