APL Antibody
Description
Definition and Classification of Antiphospholipid Antibodies (aPL)
Antiphospholipid antibodies (aPL) are autoimmune antibodies targeting phospholipid-binding proteins such as β2-glycoprotein I (β2GPI), prothrombin, annexin A2, and other coagulation regulators . These antibodies disrupt homeostasis by interfering with phospholipid-dependent coagulation pathways, increasing thrombotic risk .
Key types include:
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Lupus anticoagulant (LA): Functional coagulation assay detecting antibodies that prolong phospholipid-dependent clotting times .
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Anticardiolipin antibodies (aCL): ELISA-detected IgG/IgM antibodies targeting cardiolipin-β2GPI complexes .
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Anti-β2-glycoprotein I antibodies (aβ2GPI): Directly target β2GPI, a critical cofactor in APS pathogenesis .
Clinical Significance and Associated Conditions
aPL are central to antiphospholipid syndrome (APS), characterized by thrombosis, pregnancy morbidity, and autoimmune comorbidities .
aPL positivity is also linked to SLE, with 30%–40% of SLE patients testing positive for at least one aPL .
Prevalence and Persistence in Populations
aPL prevalence varies by population and assay methodology:
| Population | aPL Positivity Rate | Persistent Positivity Rate |
|---|---|---|
| General population | 1%–5% | 1%–2% |
| Systemic lupus erythematosus (SLE) | 30%–40% | 20% (clinically significant) |
| Patients with unprovoked DVT | 10%–17% | 6%–12% |
Persistent positivity (confirmed ≥12 weeks apart) is required for APS diagnosis . A longitudinal study found 93% of high-titer aPL patients retained positivity over 4.4 years, compared to 47% in low-titer groups .
Diagnostic Criteria and Risk Stratification
APS diagnosis requires one clinical criterion (thrombosis/pregnancy morbidity) and two positive aPL tests ≥12 weeks apart .
High-risk profiles include:
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Triple positivity (LA + aCL + aβ2GPI): 41% of APS patients; confers 37.1x higher thrombosis risk .
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Isolated LA positivity: 3.3x higher thrombosis risk vs. double-negative profiles .
| Profile | Thrombosis Risk (HR) | Obstetric Risk (OR) |
|---|---|---|
| Triple positivity | 37.1 | 12.4 |
| LA + aβ2GPI IgG | 22.5 | 8.9 |
| Isolated aCL IgM | 1.8 | 1.2 |
Emerging Research and Non-Criteria Antibodies
Recent studies highlight the role of non-criteria aPL:
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IgA isotype aβ2GPI: Associated with thrombotic APS (HR 33.9) but not obstetric complications .
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Anti-phosphatidylserine/prothrombin (aPS/PT): Present in 38% of seronegative APS cases .
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Anti-domain 1 β2GPI IgG: Strongly correlates with thrombosis (specificity 99%) and may predict APS progression .
Management and Prognostic Implications
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Primary prophylaxis: Low-dose aspirin for asymptomatic aPL carriers with high-risk profiles .
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Acute thrombosis: Heparin followed by warfarin (INR 2.0–3.0) .
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Obstetric APS: Low-molecular-weight heparin + aspirin reduces miscarriage risk by 74% .
Mortality in APS is 10%–15% at 10 years, primarily due to catastrophic APS (CAPS) or thrombotic events .
Product Specs
Constituents: 50% Glycerol, 0.01M PBS, pH 7.4
Target Background
- APL Antibody (FE protein) regulates the transcription of FT and florigen transporter genes in different manners in leaf phloem companion cells. PMID: 29036620
- The FE protein regulates the expression of FTIP1 involved in FT transport. FE protein promotes flowering through transcriptional activation of FT and Ftip1. PMID: 26239308
Q&A
FAQs for APL Antibody Research
What experimental methodologies are recommended for detecting and quantifying APL antibodies in clinical cohorts?
APL antibodies are detected using solid-phase assays (e.g., ELISA for anticardiolipin [aCL], anti-β2 glycoprotein I [aβ2GPI], and antiphosphatidylserine/prothrombin [aPS/PT]) and functional assays like lupus anticoagulant (LA) testing .
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Key steps:
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Cohort selection: Prioritize diverse populations to account for ethnic/sex-based variability in aPL prevalence .
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Assay validation: Use standardized thresholds (e.g., ≥40 units for moderate/high titers) to reduce inter-laboratory variability .
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Longitudinal sampling: Confirm persistence of aPL positivity over ≥12 weeks to distinguish transient vs pathogenic antibodies .
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How do APL antibodies contribute to thrombotic risk in autoimmune diseases?
APL antibodies activate endothelial cells, platelets, and neutrophils via interactions with phospholipid-binding proteins (e.g., β2GPI), leading to a prothrombotic state .
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Mechanistic insights:
How can researchers resolve contradictions in associations between APL subtypes and clinical outcomes?
Discrepancies arise from differences in assay sensitivity, threshold definitions, and population diversity .
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Example:
What experimental designs are optimal for studying APL-mediated endothelial dysfunction?
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In vitro models:
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In vivo models:
How should non-criteria APL antibodies (e.g., aPS/PT, IgA isotypes) be integrated into research frameworks?
Non-criteria antibodies are clinically relevant but excluded from APS classification .
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Recommendations:
What are the challenges in linking APL antibody titers to disease activity?
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Key issues:
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Solution: Perform serial measurements and apply machine learning to identify high-risk antibody profiles .
