Search for inflammatory mediators that amplify the thrombus-forming activity of antiphospholipid antibodies

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  • 全身性エリテマトーデスにおける抗リン脂質抗体の血栓形成作用を増幅させる炎症メディエーターの探索
  • ゼンシンセイ エリテマトーデス ニ オケル コウリン シシツ コウタイ ノ ケッセン ケイセイ サヨウ オ ゾウフク サセル エンショウ メディエーター ノ タンサク

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Abstract

<p>In secondary antiphospholipid syndrome (APS) associated with SLE, a wide variety of antiphospholipid antibodies appear in the blood, which cause repeated serious arterial and/or venous thrombotic complications. Our previous study revealed that IgG fractions purified from APS patients promote thrombus formation by increasing the levels of monocyte surface TF expression and inflammatory cytokine production. In this study, we investigated the effects of inflammatory and anti-inflammatory cytokines present in SLE patients’ sera on thrombus formation caused by IgG-aPLs. After pretreatment of healthy human monocytes with various cytokines, we analyzed the changes in monocyte surface TF expression levels caused by IgG-aPLs. Monocyte surface TF expression was assessed by measuring TF on the surface of CD14-positive cells by flow cytometric analysis. We found that the pretreatment of monocytes with TNF-α, IL-1β, and IL-6 caused a positive priming effect (increasing the level of TF expression in monocytes). On the other hand, the pretreatment with IL-10 caused a negative priming effect (suppression of TF expression in monocytes). In SLE patients, many components of the immune system, including monocytes, T cells, autoantibodies, and cytokines secreted by cells, are considered to be involved in the pathologic processes that underlie the development of thrombotic complications. The results of our study suggest that IgG-aPLs cause persistently high TF expression levels on monocyte surfaces by interacting with inflammatory cytokines, which may be an important mechanism in the pathogenesis of recurrent arterial and/or venous thrombotic complications peculiar to SLE patients.</p>

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