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Identification of two autoantigens recognised by circulating autoantibodies as potential biomarkers for diagnosing giant cell arteritis

1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15

 

  1. Dipartimento di Scienze Cliniche e di Comunità, Dipartimento di Eccellenza 2023-2027, University of Milan, and Istituto Nazionale Genetica Molecolare, Milan, Italy.
  2. Istituto Nazionale Genetica Molecolare, Milan, Italy.
  3. Unit of Clinical Immunology, Allergy and Advanced Biotechnologies, Azienda Unità Sanitaria Locale-IRCCS di Reggio Emilia, Reggio Emilia, Italy.
  4. Unit of Clinical Immunology, Allergy and Advanced Biotechnologies, Azienda Unità Sanitaria Locale-IRCCS di Reggio Emilia, Reggio Emilia, Italy.
  5. Unit of Rheumatology, Azienda Unità Sanitaria Locale-IRCCS di Reggio Emilia, Reggio Emilia, and University of Modena and Reggio Emilia, Modena, Italy.
  6. University of Modena and Reggio Emilia, Modena, Italy.
  7. IRCCS Istituto Auxologico Italiano, Laboratory of Immunorheumatologic Researches, Milan, Italy.
  8. Unit of Rheumatology, Azienda Unità Sanitaria Locale-IRCCS di Reggio Emilia, Reggio Emilia, and University of Modena and Reggio Emilia, Modena, Italy.
  9. Dipartimento di Scienze Cliniche e di Comunità, Dipartimento di Eccellenza 2023-2027, University of Milan, and Istituto Nazionale Genetica Molecolare, Milan, Italy.
  10. Dipartimento di Scienze Cliniche e di Comunità, Dipartimento di Eccellenza 2023-2027, University of Milan, and Department of Rheumatology, ASST PINI-CTO, Milan, Italy.
  11. Dipartimento di Scienze Cliniche e di Comunità, Dipartimento di Eccellenza 2023-2027, University of Milan, and IRCCS Istituto Auxologico Italiano, Laboratory of Immunorheumatologic Researches, Milan, Italy.
  12. Unit of Rheumatology, Azienda Unità Sanitaria Locale-IRCCS di Reggio Emilia, Reggio Emilia, and University of Modena and Reggio Emilia, Modena, Italy.
  13. Medical Center Monbijou and University of Bern, Switzerland.
  14. Istituto Nazionale Genetica Molecolare, Milan, Italy.
  15. IRCCS Istituto Auxologico Italiano, Laboratory of Immunorheumatologic Researches, Milan, Italy. pierluigi.meroni@unimi.it, p.meroni@auxologico.it

CER17931
2024 Vol.42, N°7
PI 1317, PF 1320
Rapid paper

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PMID: 38976303 [PubMed]

Received: 18/06/2024
Accepted : 21/06/2024
In Press: 28/06/2024
Published: 18/07/2024

Abstract

OBJECTIVES:
Giant cell arteritis (GCA) is a common vasculitis affecting patients aged 50 and older. GCA leads to chronic inflammation of large/medium-sized vessel walls with complications such as permanent vision loss and risk of stroke and aortic aneurysms. Early diagnosis is crucial and relies on temporal artery biopsy (TAB) and ultrasound imaging of temporal and axillary arteries. However, these methods have limitations. Serum biomarkers as autoantibodies have been reported but with inconclusive data for their use in the clinical setting. Additionally, C-reactive protein and erythrocyte sedimentation rate are non-specific and limited in reflecting disease activity, particularly in patients treated with IL-6 inhibitors. This study aimed to identify serum autoantibodies as new diagnostic biomarkers for GCA using a human protein array.
METHODS:
One commercial and one proprietary human protein array were used for antibody profiling of sera from patients with GCA (n=55), Takayasu (TAK n=7), and Healthy Controls (HC n=28). The identified candidate autoantigens were purified and tested for specific autoantibodies by ELISA.
RESULTS:
Antibodies against two proteins, VSIG10L (V-Set and Immunoglobulin Domain Containing 10 Like) and DCBLD1 (discoidin), were identified and found to be associated with GCA, with an overall prevalence of 43–57%, respectively, and high specificity as individual antibodies. A control series of TAK sera tested negative.
CONCLUSIONS:
Detecting GCA-specific autoantibodies may offer a new, non-invasive tool for improving our diagnostic power in GCA. Even though cell-mediated immune responses are crucial for GCA pathogenesis, this finding opens the way for investigating the additional role of humoral immune responses in the disease.

DOI: https://doi.org/10.55563/clinexprheumatol/0213qf

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