To evaluate the association of anti-IFI16 antibodies with peripheral vasculopathy and the predictive value of anti-IFI16 antibodies for the development or persistence of digital ulcers (DPDU) in SSc. A total of 42 SSc patients and 42 age- and sex-matched healthy controls were enrolled. Anti-IFI16 antibodies were examined by ELISA. Nailfold videocapillaroscopy (NVC) and power Doppler ultrasound (PDUS) were used to assess the micro- and macro-vascular involvement in SSc. All patients were followed up for 6 months to evaluate DPDU. Potential risk factors for DPDU were analyzed by a Firth's penalized logistic regression model. Of the 42 SSc patients enrolled, 19.05% patients were positive for anti-IFI16 antibodies, compared to a significantly low positivity rate of 4.76% in healthy controls (p < 0.001). SSc patients who were positive for anti-IFI16 antibodies manifested higher ulnar artery resistance index than anti-IFI16 negative patients (p = 0.018). Within a 6-month follow-up, 14 (33.3%) patients suffered from DPDU, and the prevalence of anti-IFI16 antibodies in patients with DPDU was 42.9%, remarkably higher than 7.1% in those without DPDU (p = 0.012). Additionally, patients with DPDU were more likely to have digital ulcers (DUs) at enrollment and manifest lower finger pulp blood flow, lower ulnar artery (UA) flow velocity, lower UA resistance index, and higher UA resistance index at baseline in comparison to patients without DPDU. Multivariate analysis further identified DUs at enrollment (OR 5.81; 95% CI 1.09-30.86; p = 0.046) and the positivity of anti-IFI16 antibody (OR 8.64; 95% CI 1.05-70.87; p = 0.045) as independent risk factors for DPDU. Presence of anti-IFI16 antibody is associated with higher UA resistance index in SSc. Multivariate analysis further identified anti-IFI16 antibody as a predictive marker for DPDU in SSc. Key Points • SSc patients who were positive for anti-IFI16 antibodies manifested higher ulnar artery resistance at baseline. • The prevalence of anti-IFI16 antibodies in patients with DPDU during the 6-month follow-up was remarkably higher than those without DPDU. • Multivariate analysis identified DUs at enrollment and anti-IFI16 antibody positivity as independent risk factors for DPDU. • Anti-IFI16 antibody is associated with peripheral vasculopathy in SSc. Multivariate analysis further identified anti-IFI16 as a predictive biomarker for the development of DUs.
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http://dx.doi.org/10.1007/s10067-024-07296-6 | DOI Listing |
Clin Rheumatol
January 2025
Department of Rheumatology, Huashan Hospital, Fudan University, No.12 Wulumuqi Zhong Road, Shanghai, 200040, China.
To evaluate the association of anti-IFI16 antibodies with peripheral vasculopathy and the predictive value of anti-IFI16 antibodies for the development or persistence of digital ulcers (DPDU) in SSc. A total of 42 SSc patients and 42 age- and sex-matched healthy controls were enrolled. Anti-IFI16 antibodies were examined by ELISA.
View Article and Find Full Text PDFClin Immunol
November 2024
Department of Rheumatology and Clinical Immunology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Autoantibodies are detected in idiopathic interstitial pneumonias (IIPs) without a clear connective tissue disease diagnosis, and their clinical significance is unclear. This study aimed to identify a novel autoantibody in IIPs. We screened 295 IIP patients using a S-methionine labeled protein immunoprecipitation assay.
View Article and Find Full Text PDFMed Clin (Barc)
April 2024
Systemic Autoimmune Diseases Unit, Internal Medicine Department, Vall d'Hebron University Hospital (HUVH), Vall d'Hebron Barcelona Hospital Campus, Barcelona, Spain.
Objectives: To determine the diagnostic value of anti-interferon gamma inducible protein 16 (IFI16) autoantibodies in systemic sclerosis (SSc) patients negative for all tested SSc-specific autoantibodies (SSc-seronegative patients) and to evaluate the clinical significance of these autoantibodies, whether isolated or in the presence of anti-centromere autoantibodies (ACA).
Methods: Overall, 58 SSc-seronegative and 66 ACA-positive patients were included in the study. All patients were tested for anti-IFI16 autoantibodies by an in-house direct ELISA.
Elife
May 2022
Johns Hopkins University School of Medicine, Division of Rheumatology, Baltimore, United States.
Background: Nucleic acid binding proteins are frequently targeted as autoantigens in systemic lupus erythematosus (SLE) and other interferon (IFN)-linked rheumatic diseases. The AIM-like receptors (ALRs) are IFN-inducible innate sensors that form supramolecular assemblies along double-stranded (ds)DNA of various origins. Here, we investigate the ALR absent in melanoma 2 (AIM2) as a novel autoantigen in SLE, with similar properties to the established ALR autoantigen interferon-inducible protein 16 (IFI16).
View Article and Find Full Text PDFJ Scleroderma Relat Disord
June 2020
Autoimmunity Research Laboratory, Research Centre of the Centre hospitalier de l'Université de Montréal, Montreal, QC, Canada.
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