Anti-β2GPI/β2GPI induced TF and TNF-α expression in monocytes involving both TLR4/MyD88 and TLR4/TRIF signaling pathways

Xie, Hong; Zhou, Hong; Weng, Haibo; Chen, Dongdong; Xia, Longfei; Wang, Ting; Yan, Jinchuan

doi:10.1016/j.molimm.2012.08.012

Cited by 46 publications

(34 citation statements)

References 38 publications

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“…activation and P-selectin expression as well as TXB 2 production. Such a conclusion has been supported by the report of Zhou [14,15], who demonstrated that mononuclear activation and tissue factor expression, which are involved in thrombosis, are induced by the anti-β 2 GP I / β 2 GP I complex but not the IgG/β 2 GP I or anti-β 2 GP I / BSA complexes.…”

Section: Discussionmentioning

confidence: 67%

Anti-β2 glycoprotein I antibodies in complex with β2 glycoprotein I induce platelet activation via two receptors: apolipoprotein E receptor 2′ and glycoprotein I bα

et al. 2015

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Anti-β2 glycoprotein I (anti-β2GPI ) antibodies are important contributors to thrombosis, especially in patients with antiphospholipid syndrome (APS). However, the mechanism by which anti-β2GPI antibodies are involved in the pathogenesis of thrombosis is not fully understood. In this report, we investigated the role of anti- β2GPI antibodies in complexes with β2GPI as mediators of platelet activation, which can serve as a potential source contributing to thrombosis. We examined the involvement of the apolipoprotein E receptor 2' (apoER2') and glycoprotein I ba (GP I ba) in platelet activation induced by the anti-β2GPI /β2GPI complex. The interaction between the anti-β2GPI /β2GPI complex and platelets was examined using in vitro methods, in which the Fc portion of the antibody was immobilized using protein A coated onto a microtiter plate. Platelet activation was assessed by measuring GPII b/III a activation and P-selectin expression and thromboxane B2 production as well as p38 mitogen-activated protein kinase phosphorylation. Our results revealed that the anti-β2GPI /β2GPI complex was able to activate platelets, and this activation was inhibited by either the anti-GP I bα antibody or the apoER2' inhibitor. Results showed that the anti-β2GPI /β2GPI complex induced platelet activation via GPI ba and apoER2', which may then contribute to the prothrombotic tendency in APS patients.

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Section: Discussionmentioning

confidence: 67%

Anti-β2 glycoprotein I antibodies in complex with β2 glycoprotein I induce platelet activation via two receptors: apolipoprotein E receptor 2′ and glycoprotein I bα

et al. 2015

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“…Shown are the representative results of three separate experiments with similar results. A B mokines promote the formation and development of atherosclerotic plaque as well as intravascular thrombi in patients with autoimmune diseases [35][36][37][38][39][40][41] . Although the involvement of cytokines and chemokines in the pathogenesis of atherosclerosis and autoimmune diseases is widely accepted, little is known about the underlying mechanisms or how these molecules trigger vascular inflammation and interact with autoantibodies.…”

Section: Discussionmentioning

confidence: 99%

Involvement of TLR4 in Oxidized LDL/β2GPI/Anti-β2GPI-Induced Transformation of Macrophages to Foam Cells

Zhang

Xie

Zhou

et al. 2014

JAT

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Aim: It has been reported that oxidized low-density lipoprotein (oxLDL) forms a stable and non-dissociable complex with β2-glycoprotein I (β2GPI) and that IgG anti-β2GPI autoantibodies are able to recognize this complex, thus facilitating macrophage-derived foam cell formation in patients with antiphospholipid syndrome (APS). However, the immunopathological mechanisms of oxLDL/β2GPI complexes in promoting foam cell formation are not fully understood. In this study, we examined the role of toll-like receptor 4 (TLR4) in the oxLDL/β2GPI/anti-β2GPI complex-induced transformation of mouse peritoneal macrophages to foam cells.

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“…Studies of the human monocytic THP-1 cell line have shown that incubation with rabbit anti-β 2 GPI/β 2 GPI complexes increased TF mRNA expression, TF activity, and expression of TLR4, MyD88, and myeloid differentiation protein-2, a critical cofactor that interacts with TLR4 24. Recently, the same group showed that treatment of healthy ex vivo monocytes or THP-1 cells with monoclonal anti-β 2 GPI/β 2 GPI complexes increased MyD88 and TRIF mRNA and protein expression and this effect was blocked by addition of TAK-242, a blocker of signalling transduction mediated by the intracellular domain of TLR4 25. To our knowledge, we are the first to identify the involvement of TRIF in APS TLR4-mediated trophoblast signalling.…”

Section: Discussionmentioning

confidence: 99%

Purified IgG from Patients with Obstetric but not IgG from Non‐obstetric Antiphospholipid Syndrome Inhibit Trophoblast Invasion

Poulton

Ripoll

Pericleous

et al. 2014

American J Rep Immunol

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ProblemSome patients with antiphospholipid syndrome (APS) suffer pregnancy morbidity (PM) but not vascular thrombosis (VT), whilst others suffer VT only. Therefore, we compared the effects of IgG from VT+/PM− and VT−/PM+ subjects on human first-trimester trophoblast (HTR8) cells.Method of studyHTR-8 cells were incubated with APS VT+/PM−, APS VT−/PM+ or healthy control (HC) IgG. We measured trophoblast invasion by cell invasion assay; mRNA expression of TLR4 and adaptor proteins; phosphorylation of p38 MAPK, NFκB and ERK; and expression of interleukin (IL)-8 and IL-6.ResultsVT−/PM+ IgG, but not VT+/PM− IgG significantly reduced HTR-8 invasion. The effects on invasion were blocked by TLR-4 inhibition. Neither VT+/PM− nor VT−/PM+ IgG altered MyD88 mRNA expression, phosphorylation of signalling molecules or cytokine expression.ConclusionsVT−/PM+ IgG exert functionally relevant effects on human trophoblast cells but VT+/PM− IgG do not.

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Anti-β2GPI/β2GPI induced TF and TNF-α expression in monocytes involving both TLR4/MyD88 and TLR4/TRIF signaling pathways

Cited by 46 publications

References 38 publications

Anti-β2 glycoprotein I antibodies in complex with β2 glycoprotein I induce platelet activation via two receptors: apolipoprotein E receptor 2′ and glycoprotein I bα

Anti-β2 glycoprotein I antibodies in complex with β2 glycoprotein I induce platelet activation via two receptors: apolipoprotein E receptor 2′ and glycoprotein I bα

Involvement of TLR4 in Oxidized LDL/β2GPI/Anti-β2GPI-Induced Transformation of Macrophages to Foam Cells

Purified IgG from Patients with Obstetric but not IgG from Non‐obstetric Antiphospholipid Syndrome Inhibit Trophoblast Invasion

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