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These are lupus anticoagulant (LA), anticardiolipin antibodies (aCL) and anti-beta-2 glycoprotein I antibodies (anti-B2GPI). This review will focus on anti-B2PI and their role in APS in terms of their relationship to the putative pathogenesis of the disorder and their clinical associations.
- The role of beta-2-glycoprotein I in health and disease associating ...
Coagulation and Complement Interactions. This diagram shows...
- The role of beta-2-glycoprotein I in health and disease associating ...
Coagulation and Complement Interactions. This diagram shows the varying contrasting interactions of CRP, thrombomodulin and beta-2-glycoprotein I. Red arrows indicate upregulation in the presence of β2GPI whilst red arrows with a circular ending indicate inhibition in the presence of β2GPI.
12 lip 2012 · The discovery that the anticardiolipin antibodies that are correlated with thrombotic complications are in reality autoantibodies that recognize β 2 GPI, which has a high affinity for cardiolipin, has been an important improvement in the development of diagnostics for the syndrome.
Anti-beta 2 glycoprotein 1 (anti-β2GP1) antibodies are commonly found in patients with autoimmune diseases such as the antiphospholipid syndrome (APS) and systemic lupus erythematosus (SLE). Their presence is highly associated with increased risk of ...
1 sie 2019 · Chemiluminescent assays (CLIA) can be used as an alternative to ELISA. Recent advances allow us to propose antibodies targeting beta-2-glycoprotein I (β 2 -GPI) as the most specific antibodies associated with anti-phospholipid syndrome (APS).
14 paź 2021 · Anti-beta 2 glycoprotein I antibodies in a general obstetric population: preliminary results on the prevalence and correlation with pregnancy outcome. Anti-beta2 glycoprotein I antibodies are associated with some obstetrical complications, mainly preeclampsia-eclampsia.
4 lis 2021 · Effects of beta 2-glycoprotein 1 antibodies on different cellular targets and their damage-generating pathways (A) aß2GP1 pro-inflammatory effect via TLR4/Myd88. (B) aß2GP1 induced a reduction in the promigratory effect of IL6 and STAT3.