TNF-alpha and annexin A2: inflammation in thrombotic primary antiphospholipid syndrome

Abstract

Antiphospholipid syndrome (APS) is characterized by thromboses and/or pregnancy losses. Laboratory criterion for the diagnosis of APS is the presence of antiphospholipid antibodies (anticardiolipin, anti-beta2-glycoprotein I (aβ2gpI) and lupus anticoagulant). On the one hand, the latest classification criteria for the diagnosis of APS emphasized that thrombotic manifestations of the syndrome should be without any signs of an inflammatory process, while on the other hand, some recent reports have suggested that APS is a "pro-inflammatory state." This article is focused on the importance of TNF-alpha and annexin A2 (anxA2) for patients with vascular (thrombotic) manifestations of the primary APS. The classic antithrombotic and antiplatelet therapy does not protect APS patients from the development of recurrent thrombosis. Therefore, an urgent need for the introduction of new therapeutic approaches in the treatment of APS patients is obvious. This review provides a rationale for the necessity for the use of immunomodulatory medications that could interfere with β2gpI binding to its receptor(s), such as anxA2, and/or inhibit TNF-alpha activity.

The relationship between inflammatory mediator expression in the aqueous humor and secondary glaucoma incidence after silicone oil tamponade

“…Neutrophils and macrophages could worsen inflammation primarily by secreting IL-6, TNF-α and other factors ( 22 ). TNF-α is directly involved in induction of apoptosis and could destroy the function of the trabecular cells ( 23 ). IL-6 is a pleiotropic factor which can induce the expression of a variety of inflammatory mediators and the activation of lymphocytes and NK cells, thus, exacerbating inflammation ( 24 ).…”

Annexin A2: The diversity of pathological effects in tumorigenesis and immune response

“…99 Researchers have found that in APLS patients with thrombosis, ANXA2 can be used as a receptor binding to β2gpI, promoting serum tumor necrosis factor alpha (TNF-α) activity and thrombosis. 100 According to an earlier study, serum levels of anti-ANXA2 antibodies in patients with APLS were significantly elevated, and anti-ANXA2 antibodies and antiphospholipid antibodies were negatively correlated. 101 A study in 2021 revealed that the level of anti-ANXA2 antibodies in APLS patients was significantly higher than that in normal control subjects, and the thrombosis rate was significantly increased in mouse models with elevated anti-ANXA2 antibodies.…”

“…Antiphospholipid syndrome (APLS) is an autoimmune disorder characterized by increased thrombosis and anti‐beta2‐glycoprotein I (β2gpI) antibody production 99 . Researchers have found that in APLS patients with thrombosis, ANXA2 can be used as a receptor binding to β2gpI, promoting serum tumor necrosis factor alpha (TNF‐α) activity and thrombosis 100 . According to an earlier study, serum levels of anti‐ANXA2 antibodies in patients with APLS were significantly elevated, and anti‐ANXA2 antibodies and antiphospholipid antibodies were negatively correlated 101 .…”

Hyperoside Protects Human Umbilical Vein Endothelial Cells Against Anticardiolipin Antibody-Induced Injury by Activating Autophagy

“…Antiphospholipid syndrome (APS) is a rare systemic autoimmune disorder clinically characterized by recurrent thrombosis or pregnancy morbidity in combination with the persistent presence of circulating antiphospholipid antibody (aPL), including anticardiolipin antibody (aCL), anti-b2glycoprotein I (anti-b2GPI), and lupus anticoagulant (LA) (Woo et al, 2010;Gomez-Puerta and Cervera, 2014;Linnemann, 2018). Various mechanisms have been speculated to contribute to the disease progression regarding to inflammation (Becarevic, 2016), adhesion receptors (Lopez-Pedrera et al, 2017), oxidative stress (Benhamou et al, 2015), and neutrophil extracellular traps (Meng et al, 2017) in APS patients. Usually, APS patients have a greater predisposition to cardiovascular disorders, involving coronary artery disease, myocardial infarction, and stroke (Kolitz et al, 2019).…”