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抗严重急性呼吸综合征冠状病毒 2 腺病毒载体疫苗引发亚临床抗血小板自身免疫和可溶性血小板活化标志物增加。

Anti-severe acute respiratory syndrome coronavirus-2 adenoviral-vector vaccines trigger subclinical antiplatelet autoimmunity and increase of soluble platelet activation markers.

机构信息

Section of Internal and Cardiovascular Medicine, University of Perugia, Perugia, Italy.

Section of Occupational Medicine and Toxicology, University of Perugia, Perugia, Italy.

出版信息

Br J Haematol. 2022 Jul;198(2):257-266. doi: 10.1111/bjh.18245. Epub 2022 May 16.

Abstract

To slow down the coronavirus disease 2019 (COVID-19) pandemic an unequalled vaccination campaign was initiated. Despite proven efficacy and safety, a rare but potentially fatal complication of adenoviral-vector vaccines, called vaccine-induced immune thrombotic thrombocytopenia (VITT), has emerged the pathogenesis of which seems to be related to the development of platelet-activating anti-platelet factor 4 (PF4) antibodies. While a few studies have evaluated the incidence of anti-PF4 positivity in anti-severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) vaccine recipients, to date no studies have assessed whether an antiplatelet immunological response develops and if this associates with platelet and blood clotting activation. We carried out a prospective study in healthy subjects who received the first dose of ChAdOx1 or Ad26.COV2.S or BNT162b2 vaccines to evaluate platelet-specific and non-specific immune response and in vivo platelet activation and blood clotting activation. Individuals receiving ChAdOx1 and, less so, Ad26.COV2.S developed with high frequency auto- or alloantiplatelet antibodies, increased circulating platelet-derived microvesicles and soluble P-selectin associated with mild blood clotting activation. Our study shows that an immunological reaction involving platelets is not uncommon in individuals receiving anti-SARS-CoV-2 vaccination, especially after ChAdOx1 and Ad26.COV2.S, and that it associates with in vivo platelet and blood clotting activation.

摘要

为了减缓 2019 年冠状病毒病(COVID-19)大流行,启动了一场前所未有的疫苗接种运动。尽管腺病毒载体疫苗已被证明具有疗效和安全性,但一种罕见但可能致命的并发症——疫苗诱导的免疫性血栓性血小板减少症(VITT)已经出现,其发病机制似乎与血小板激活抗血小板因子 4(PF4)抗体的产生有关。虽然有几项研究评估了抗严重急性呼吸综合征冠状病毒 2(SARS-CoV-2)疫苗接种者中抗 PF4 阳性的发生率,但迄今为止,尚无研究评估是否会发生抗血小板免疫反应,以及这种反应是否与血小板和凝血激活有关。我们在接受 ChAdOx1 或 Ad26.COV2.S 或 BNT162b2 疫苗第一剂的健康受试者中进行了一项前瞻性研究,以评估血小板特异性和非特异性免疫反应以及体内血小板激活和凝血激活。接受 ChAdOx1 疫苗接种的个体(尤其是 Ad26.COV2.S 疫苗接种者)会高频产生自身或同种异体抗血小板抗体,循环血小板衍生的微泡增加,可溶性 P-选择素增加,与轻度凝血激活相关。我们的研究表明,在接受 SARS-CoV-2 疫苗接种的个体中,涉及血小板的免疫反应并不罕见,尤其是在接受 ChAdOx1 和 Ad26.COV2.S 疫苗接种后,并且与体内血小板和凝血激活有关。

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