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Could the IgA isotype provide additional information in systemic sclerosis patients? A retrospective study entailing IgA isotyping in a Mediterranean systemic sclerosis cohort


1, 2, 3, 4, 5, 6, 7, 8, 9, 10

 

  1. Department of Immunology, Centre de Diagnòstic Biomèdic (CDB), Hospital Clínic, Barcelona, and Institut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain.
  2. Institut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona; Department of Autoimmune Diseases, Hospital Clínic, University of Barcelona, Barcelona; and Reference Centre for Systemic Autoimmune Diseases (CSUR) of the Spanish Health System, Barcelona, Spain.
  3. Department of Immunology, Centre de Diagnòstic Biomèdic (CDB), Hospital Clínic, Barcelona, Spain.
  4. Department of Immunology, Centre de Diagnòstic Biomèdic (CDB), Hospital Clínic, Barcelona, Spain.
  5. Department of Immunology, Centre de Diagnòstic Biomèdic (CDB), Hospital Clínic, Barcelona, Spain.
  6. Institut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona; Department of Autoimmune Diseases, Hospital Clínic, University of Barcelona, Barcelona; and Reference Centre for Systemic Autoimmune Diseases (CSUR) of the Spanish Health System, Barcelona, Spain.
  7. Thermo Fisher Scientific, Cornellà de Llobregat, Spain.
  8. Thermo Fisher Scientific, Freiburg, Germany.
  9. Department of Immunology, Centre de Diagnòstic Biomèdic (CDB), Hospital Clínic, Barcelona, and Institut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain. ovinyas@clinic.cat
  10. Department of Immunology, Centre de Diagnòstic Biomèdic (CDB), Hospital Clínic, Barcelona, and Institut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain. esruiz@clinic.cat

CER16934
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PMID: 37812465 [PubMed]

Received: 21/06/2023
Accepted : 26/09/2023
In Press: 29/09/2023

Abstract

OBJECTIVES:
Anti-CENP-B (ACA), anti-topoisomerase I (ATA) and anti-RNA polymerase III (RP3) autoantibodies are included in the 2013 SSc-ACR/EULAR classification criteria. The detection of additional autoantibodies is of interest when those are negative. Additionally, we wonder if the IgA isotype might play a role in SSc. The aims of the study were to assess the prevalence of ACA, ATA, RP3, and Ro52 autoantibodies of IgG and IgA isotype and to describe their association with clinical manifestations in a cohort of patients with SSc.
METHODS:
Samples from 97 patients with SSc fulfilling the 2013 ACR/EULAR classification criteria, and 50 blood donors were included and tested for IgA and IgG isotypes of ACA, ATA, RP3, and Ro52 by FEIA.
RESULTS:
The prevalence of IgG+IgA isotypes for the same specificity was 62.5%, 82.6%, 80.0%, 36.8%, for ACA, ATA, RP3 and Ro52, respectively. Isolated IgG was present in 35.4%, 13.0%, 20.0% and 42.1% of patients for ACA, ATA, RP3 and Ro52, respectively. Only six patients were isolated IgA for a unique specificity. Clinically, ILD tended to be associated with ATA-IgG and ATA-IgG+IgA, telangiectasias with ACA-IgG+IgA and arthritis with ACA-IgA. Indeed, digital ulcers were more frequent in ATA-IgG patients.
CONCLUSIONS:
Most of the patients presented ACA, ATA, or RP3 autoantibodies of IgA isotype in addition to IgG. Regarding clinical relevance, Ro52-IgG+IgA and ACA-IgG had a tendency towards sineSSc phenotype, while ACA-IgG+IgA to lcSSc phenotype. Thus, if confirmed, the determination of ACA-IgA could provide a tool to stratify patients according to the cutaneous phenotype.

DOI: https://doi.org/10.55563/clinexprheumatol/qijvcj

Rheumatology Article