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首页> 外文期刊>Journal of Hepatology: The Journal of the European Association for the Study of the Liver >Anti-phospholipid antibodies associated with alcoholic liver disease target oxidized phosphatidylserine on apoptotic cell plasma membranes.
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Anti-phospholipid antibodies associated with alcoholic liver disease target oxidized phosphatidylserine on apoptotic cell plasma membranes.

机译：与酒精性肝病相关的抗磷脂抗体靶向凋亡细胞质膜上的氧化磷脂酰丝氨酸。

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BACKGROUND/AIMS: Circulating anti-phospholipid antibodies (aPL) are often present in patients with alcoholic liver disease (ALD). The observations that defects in the disposal of apoptotic corpses leads to the development of aPL prompted us to investigate whether ALD-associated aPL might recognize antigens in apoptotic cells. METHODS: Apoptosis was induced in HuT-78 human T-lymphoma and HepG2 hepatoma cells by, respectively, FAS ligation with CH11 monoclonal antibodies or the incubation with ethanol (400 mmol/L). RESULTS: Flow cytometry revealed that IgG from ALD patients with high aPL titers selectively bind to the surface of apoptotic, but not to viable cells. No binding was instead evident using either control or aPL-negative ALD sera. ELISA assays using different oxidized phospholipids as antigens showed that anti-phospholipid reactivity of ALD sera was mainly directed towards oxidized cardiolipin and phosphatidylserine. The pre-adsorption of aPL-positive sera with oxidized phosphatidylserine, but not with oxidized cardiolipin, lowered aPL binding to apoptotic HuT-78 cells by about 50%. No effect was instead observed by pre-adsorption with oxidation-protected phospholipids or with human serum albumin adducted with different lipid peroxidation products. CONCLUSIONS: aPL associated with ALD target apoptotic cells by specifically recognizing oxidized phosphatidylserine, suggesting a possible link between hepatocyte apoptosis and anti-phospholipid auto-reactivity in ALD.
机译：背景/目的：酒精性肝病（ALD）患者中经常存在循环抗磷脂抗体（aPL）。凋亡小体的处置缺陷导致aPL的发展的发现促使我们研究与ALD相关的aPL是否可以识别凋亡细胞中的抗原。方法：通过FAS连接CH11单克隆抗体或用乙醇（400 mmol / L）孵育，分别在HuT-78人T淋巴瘤和HepG2肝癌细胞中诱导凋亡。结果：流式细胞仪显示，来自aPL滴度高的ALD患者的IgG选择性结合凋亡的表面，但不结合活细胞。相反，使用对照或aPL阴性ALD血清均未发现明显的结合。使用不同的氧化磷脂作为抗原的ELISA分析表明，ALD血清的抗磷脂反应性主要针对氧化的心磷脂和磷脂酰丝氨酸。用氧化的磷脂酰丝氨酸而不是用氧化的心磷脂预吸附aPL阳性血清，可使aPL与凋亡的HuT-78细胞的结合降低约50％。相反，通过用氧化保护的磷脂或与不同脂质过氧化产物加成的人血清白蛋白的预吸附，未观察到任何作用。结论：aPL通过特异性识别氧化的磷脂酰丝氨酸与ALD靶向凋亡细胞，提示ALD中肝细胞凋亡与抗磷脂自身反应性之间可能存在联系。

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