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Anti-Nuclear Antibody Screening Using HEp-2 Cells
Published on: June 23, 2014
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Bicaudal D2 autoantibodies are highly specific for systemic sclerosis
L V Iversen1,2,3, C Tandrup Nielsen3,4, S Jacobsen4
1Department of Dermatology, Odense University Hospital, Odense, Denmark.
Scandinavian Journal of Rheumatology
|June 24, 2024
Summary
Autoantibodies against bicaudal D2 (BICD2) are highly specific markers for systemic sclerosis (SSc). Their presence in SSc patients correlates with altered lung function, suggesting a role in disease pathophysiology.
Area of Science:
- Immunology
- Rheumatology
- Pulmonology
Background:
- Autoantibodies against intracellular proteins can serve as specific biomarkers for autoimmune diseases.
- Bicaudal D2 (BICD2) protein autoantibodies (anti-BICD2) have been identified as a potential marker for systemic sclerosis (SSc).
Purpose of the Study:
- To determine the prevalence of anti-BICD2 in a cohort of patients with connective tissue diseases (CTDs) and healthy controls.
- To evaluate the clinical and laboratory associations of anti-BICD2 in SSc patients.
Main Methods:
- A cross-sectional study involving 363 patients with CTDs (including SSc, systemic lupus erythematosus, and myositis) and 100 blood donors.
- Testing for anti-BICD2 and specific anti-nuclear antibodies (ANAs) in SSc patients.
- Clinical and laboratory data analysis stratified by anti-BICD2 status.
Main Results:
- Anti-BICD2 was detected in 35 out of 121 SSc patients, showing 96.5% specificity but only 28.9% sensitivity for SSc.
- Anti-BICD2 frequently co-occurred with centromere autoantibodies in SSc patients (91%).
- Anti-BICD2-positive SSc patients exhibited significantly lower forced expiratory volume in 1 second (FEV1) and carbon monoxide transfer coefficient (KCO), but higher forced vital capacity.
Conclusions:
- Autoantibodies against BICD2 are highly specific for systemic sclerosis.
- The association of anti-BICD2 with reduced FEV1 and KCO suggests a link to altered lung function in SSc, warranting further investigation into the underlying pathophysiological mechanisms.
