These criteria have limitations in that they omit nonclassical manifestations (hematologic and neurologic), include anticardiolipin and anti-β2-glycoprotein I immunoglobulin (Ig)M isotypes, and do not separately consider primary (no autoimmune disease) or secondary (usually systemic lupus erythematosus) disease.
These antibodies, albeit at concentrations exceeding those generally found in periodontitis subjects, are typically present in patients with the antiphospholipid syndrome (APS), an autoimmune disease characterized by thrombosis and recurrent pregnancy loss. aCL from APS patients are proinflammatory and can activate trophoblasts, macrophages, and platelets via cell-surface interactions with their target antigen beta-2-glycoprotein-I (β2GPI).
This feature may lead to two major events: i) immunization with β2GPI fosters the Fc-receptor-mediated uptake by antigen presenting cells of apoptotic material decorated with β2GPI and the activation of β2GPI-specific T cells which in turn provide help to β2GPI-specific B cells for the production of anti-β2GPI; ii) apoptotic bodies decorated with β2GPI can be opsonized by anti-β2GPI and shifted towards a pro-inflammatory clearance by macrophages; epitope spread can occur with the generation of autoimmunity against nuclear autoantigens.
β2 -Glycoprotein I (β2 -GPI), also designated apolipoprotein H, is a 50-kDa protein that circulates in blood at high concentrations, playing important roles in autoimmune diseases, hemostasis, atherogenesis, and angiogenesis, as well as in host defense against bacteria and in protein/cellular waste removal.
To investigate cloning and expression of beta 2-glycoprotein 1 (beta 2GP1) recognized by antiphospholipid antibodies and to study the clinical significance of anti-beta 2GP1 antibodies in patients with autoimmune disease.