LAC13 antibodies (associated with lupus anticoagulant activity) are typically detected using:
Solid-phase immunoassays: ELISA for anti-β2-glycoprotein I (anti-β2-GPI) or anticardiolipin (aCL) antibodies .
Functional coagulation assays: Dilute Russell’s viper venom time (dRVVT) or activated partial thromboplastin time (aPTT) following ISTH guidelines to confirm lupus anticoagulant (LAC) activity .
Statistical validation: Mann-Whitney U tests for cohort comparisons (e.g., thrombotic vs. non-thrombotic patients) .
In vitro: Transfect LAD cells with siRNA targeting thrombotic pathways (e.g., GLUT1) to assess antibody interactions .
In vivo: Use murine models immunized with antigen-depleted plasma to study antibody production and thrombotic outcomes .
LAC13 antibodies target β2-glycoprotein I (β2-GPI) and exhibit:
Higher thrombotic risk: Associated with arterial/venous events in COVID-19 and APS patients .
Isotype specificity: IgA/IgG anti-β2-GPI antibodies correlate with severe thrombotic outcomes compared to IgM .
Discrepancies arise from differences in:
A multi-step workflow is recommended:
Immunoaffinity purification: Use mAbs to pull down target antigens from plasma .
Proteomic validation: SDS-PAGE/Western blotting followed by mass spectrometry (e.g., shotgun proteomics) .
Functional characterization: ELISA-based quantification of antigen levels (e.g., Haptoglobin β at ~120 ng/mL in NSCLC plasma) .
Transcriptomics: Identify upregulated pathways (e.g., PI3K/GLUT1 in LAD cells) linked to antibody-mediated thrombosis .
Proteomics: Detect low-abundance antigens (e.g., residual Haptoglobin β at <5% post-depletion) in immunized models .
Transient positivity: ~50% of LAC-positive COVID-19 patients revert to negative status within 4 weeks .
Confounding factors: Pre-existing cardiovascular disease or inflammatory states elevate LAC titers independently of thrombosis .