**Background of Anti-Plasminogen (PLG) Antibodies**
Plasminogen (PLG), a glycoprotein synthesized in the liver, is a central component of the fibrinolytic system. It circulates as an inactive precursor and is converted to plasmin, an enzyme that degrades fibrin clots, facilitating thrombosis resolution and tissue remodeling. Dysregulation of plasminogen activation is linked to thrombotic disorders, bleeding tendencies, and inflammatory conditions.
Anti-PLG antibodies, autoantibodies targeting plasminogen, have been implicated in various pathologies. In autoimmune diseases like systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS), these antibodies may interfere with fibrinolysis, contributing to thrombotic events or recurrent pregnancy loss by disrupting plasmin-mediated processes. They are also observed in infections (e.g., streptococcal) where molecular mimicry may trigger autoimmunity.
Clinically, anti-PLG antibodies are detected via ELISA or immunoblotting. Their presence correlates with disease activity in some autoimmune conditions, though their pathogenic role remains debated. Research explores their utility as biomarkers for thrombosis risk or therapeutic monitoring. Treatment often focuses on managing underlying conditions, with anticoagulants or immunosuppressants considered in refractory cases.
Understanding anti-PLG antibodies highlights the interplay between coagulation, immunity, and inflammation, offering insights into novel diagnostic and therapeutic strategies for thrombotic and autoimmune disorders.