The role of tissue factor in the antiphospholipid syndrome

Dobado‐Berrios, Pablo‐Manuel; López-Pedrera, C.; Velasco, Francisco; Cuadrado, M J

doi:10.1002/1529-0131(200111)44:11<2467::aid-art426>3.0.co;2-u

Cited by 47 publications

(30 citation statements)

References 99 publications

(171 reference statements)

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“…32 Numerous reports have demonstrated that plasma from patients with the APS contains antibodies that bind and activate endothelial cells, 15,33 and that endothelial cell activation may occur in a ␤ 2 GPI-dependent manner. 17,22 The clinical relevance of endothelial cell activation in patients with the APS is supported by reports demonstrating increased circulating levels of tissue factor 34 and VCAM-1, 35 as well as endothelial microparticles, 36 in these individuals.…”

Section: Discussionmentioning

confidence: 90%

Annexin A2 mediates endothelial cell activation by antiphospholipid/anti-β2 glycoprotein I antibodies

Zhang

McCrae

2005

Blood

212

203

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Patients with antiphospholipid antibodies (APLAs) are at increased risk for arterial and venous thrombosis. Many APLAs associated with these events react with ␤ 2 glycoprotein I (␤ 2 GPI), and endothelial cell reactive antibodies that activate endothelial cells in a ␤ 2 GPI-dependent manner occur commonly in these patients. We previously reported that ␤ 2 GPI binds with high affinity to annexin A2 on the endothelial surface, though the relevance of this interaction to APLA/anti-␤ 2 GPI antibodyinduced endothelial activation has not been determined. In this report, we confirm that anti-␤ 2 GPI antibodies activate endothelial cells in the presence of ␤ 2 GPI, and demonstrate that anti-annexin A2 antibodies directly cause endothelial cell activation of a similar magnitude and with a similar time course. Moreover, bivalent anti-annexin A2 F(ab) 2 fragments also caused endothelial cell activation, whereas monomeric Fab fragments not only did not cause activation, but blocked activation induced by anti-annexin A2 antibodies and F(ab) 2 fragments, as well as that caused by anti-␤ 2 GPI antibodies in the presence of ␤ 2 GPI. These observations suggest a novel pathway for endothelial activation induced by APLA/anti-␤ 2 GPI antibodies that is initiated by crosslinking or clustering of annexin A2 on the endothelial surface. (Blood. 2005;105: 1964-1969

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Section: Discussionmentioning

confidence: 90%

Annexin A2 mediates endothelial cell activation by antiphospholipid/anti-β2 glycoprotein I antibodies

Zhang

McCrae

2005

Blood

212

203

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“…27 An anticardiolipin antibody-mediated increase in tissue factor expression contributes to thrombosis in patients with the antiphospholipid syndrome. 28 In rat cardiac allografts, tissue factor plays a critical role in clotting abnormalities and transplant arteriosclerosis. 29 Lesions in allografts in rats infused with AT 1 -receptor antibodies resemble those observed in kidney-transplant recipients.…”

Section: Discussionmentioning

confidence: 99%

Angiotensin II Type 1–Receptor Activating Antibodies in Renal-Allograft Rejection

Dragun

Müller

Bräsen³

et al. 2005

N Engl J Med

781

684

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“…Patients with AT 1 R-Ab-mediated AMR develop small artery thrombosis and positive tissue factor staining on renal biopsies along with renal cortical infarcts on magnetic resonance imaging [4]. Tissue factor has also been associated with thrombosis in antiphospholipid syndrome and with clotting abnormalities in cardiac allografts [10,11]. Additionally, in animal models, AT 1 RAbs cause renal artery constriction in the setting of renal transplantation [12], which along with an increase in tissue factor expression, may have contributed to renal artery thrombosis in our patient's allograft.…”

Section: Discussionmentioning

confidence: 99%

Accelerated rejection, thrombosis, and graft failure with angiotensin II type 1 receptor antibodies

et al. 2015

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This case highlights the risk of allograft thrombosis associated with AT1R-Abs and illustrates that previous treatments utilized for AT1R-Abs may not always be effective. Further studies are needed to better characterize the mechanisms of AT1R-Ab pathogenesis and to establish safe levels of AT1R-Abs both pre- and post-transplantation. Given the outcome of this patient and the evidence of pro-coagulatory effects of AT1R-Abs, we suggest that the presence of AT1R-Ab may be a risk factor for thrombosis. The role of treatment with anti-coagulation and novel immunomodulatory agents such as tocilizumab and bortezomib require further investigation.

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The role of tissue factor in the antiphospholipid syndrome

Cited by 47 publications

References 99 publications

Annexin A2 mediates endothelial cell activation by antiphospholipid/anti-β2 glycoprotein I antibodies

Annexin A2 mediates endothelial cell activation by antiphospholipid/anti-β2 glycoprotein I antibodies

Angiotensin II Type 1–Receptor Activating Antibodies in Renal-Allograft Rejection

Accelerated rejection, thrombosis, and graft failure with angiotensin II type 1 receptor antibodies

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