Pathogenesis of the antiphospholipid syndrome: An additional example of the mosaic of autoimmunity

Chemical synthesis and characterization of wild‐type and biotinylated N‐terminal domain 1–64 of β2‐glycoprotein I

“…6,22 To date, the only treatment proven to reduce the risk of thrombosis in APS is life-long anticoagulation, which often has severe side effects. 3 Despite antithrombotic therapy, a significant proportion of patients with APS undergo rethrombosis, 41 likely because anticoagulant therapy affects only the final outcome, without interfering with the early biochemical events from which thrombotic events originate, that is production of anti-b2GpI Abs and binding to b2GpI.…”

“…[19][20][21] Even though it is still unclear which of these mechanisms is actually predominant in vivo, it is widely accepted that they are all affected by the presence of anti-b2GpI aAbs. 19,22,23 Hence, the possibility to find out a molecule which is able to effectively compete with b2GpI for the binding to antib2GpI aAbs, without eliciting the cellular effects mediated by anti-b2GpI Abs, would be a promising approach for developing safer therapeutic strategies in APS. 19 On the other hand, the presence of pathogenic and nonpathogenic aAbs recognizing several distinct regions of b2GpI in the plasma of APS patients, 18 from Domain I to Domain V, has impaired so far the development of reliable immunochemical tools for the diagnosis of APS.…”

Antiphospholipid Syndrome: Changing Knowledge During the Time – The ”Four P” Pattern

“…The same is true for the attempt to only list important researchers on the field. The compact overview bring Giannakopoulos or Meroni (Meroni PL;. The role of prothrombotic and proinflammatory phenotype of endothelial cells, monocytes and platelets via direct action of antiphosholipid antibodies has been summarised by Pierangelli (Pierangelli SS, et al;.…”

Experimental evidence on the immunopathogenesis of primary biliary cirrhosis

“…64,65 Autoantibodies Circulating AMAs are highly specific for PBC and are detected in nearly 100% of patients when tested for using techniques based on recombinant mitochondrial antigens (immunoblotting or enzymelinked immunosorbent assay). The high sensitivity and specificity of AMAs make them one of the most specific diagnostic tests of human immunopathology, 66 different from other autoimmune conditions, 67,68 including autoimmune hepatitis. 69 In most clinical settings for initial screening, AMAs are usually detected by indirect immunofluorescence using rodent liver, kidney and stomach sections as a substrate, leading in some cases to false positive or negative results.…”