[血小板去氟化、凋亡与血小板同种抗体和CD8+ T细胞在血小板输注难耐中的相关性分析]。

Q4 Medicine
Yan Zhou, Li-Yang Liang, Chang-Shan Su, Hui-Hui Mo, Ying Chen, Fang Lu, Yu-Chen Huang, Zhou-Lin Zhong
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引用次数: 0

摘要

目的:探讨血小板输注难耐(PTR)患者血小板同种异体抗体和CD8+ T细胞与血小板脱氮和凋亡的关系。方法:检测135例PTR患者和260例健康对照者血小板中RCA-1、CD62P和Neu1的表达。观察抗hla抗体组、抗cd36抗体组和抗体阴性组PTR患者血清诱导血小板去脂酰化和凋亡的能力,以及FcγR抑制剂对血小板去脂酰化和凋亡的潜在影响。此外,我们还分析了CD8+ T细胞与患者血小板脱氮化之间的关系。结果:PTR患者血小板中RCA-1和Neu1的表达显著高于健康供者(P < 0.05),但与血小板同种异体抗体的表达无关(P < 0.05)。PTR患者血清普遍诱导血小板体外去脂化(P < 0.05),各组间差异无统计学意义(P < 0.05)。体外实验中,抗cd36抗体组对血小板凋亡的诱导作用显著高于抗hla抗体组和抗体阴性组(P < 0.05)。在有抗cd36抗体的PTR患者中,血小板凋亡依赖于FcγR信号,而去脂酰化不依赖于FcγR信号。PTR患者CD8+ T细胞水平与血小板去脂化水平有显著相关性(P < 0.05)。结论:血小板脱氮化是PTR患者常见的病理现象,涉及CD8+ T细胞的参与,但与血小板同种抗体无关;而抗cd36抗体在预测PTR患者血小板凋亡方面具有潜在的临床意义。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Analysis of Correlation between Platelet Desialylation, Apoptosis and Platelet Alloantibody and CD8+ T Cells in Platelet Transfusion Refractoriness].

Objective: To investigate the correlation between platelet alloantibodies and CD8+ T cell with platelet desialylation and apoptosis in platelet transfusion refractoriness(PTR).

Methods: The expression of RCA-1, CD62P and Neu1 on platelets were detected in 135 PTR patients and 260 healthy controls. The ability of PTR patients' sera with anti-HLA antibody, anti-CD36 antibody and antibody-negative groups to induce platelet desialylation and apoptosis, and the potential effect of FcγR inhibitors on desialylation and apoptosis were evaluated. Additionally, the association between CD8+ T cells and platelet desialylation in patients was analyzed.

Results: The expression of RCA-1 and Neu1 on platelets in PTR patients were significantly higher than those in healthy donors(P < 0.05), but were not related to platelet alloantibody (P >0.05). The sera of PTR patients generally induced platelet desialylation in vitroP < 0.05), with no significant differences among the groups(P >0.05). However, the sera with anti-CD36 antibodies could induce platelet apoptosis significantly higher than that in the anti-HLA antibody group and antibody-negative group in vitro (P < 0.05). In PTR patients with anti-CD36 antibodies, platelet apoptosis was dependent on FcγR signaling, while desialylation is not. Moreover, CD8+ T cells in PTR patients were significantly associated with platelet desialylation (P < 0.05).

Conclusion: Platelet desialylation is a common pathological phenomenon in PTR patients, which involves the participation of CD8+ T cell, but isn't associated with platelet alloantibody; while anti-CD36 antibodies have potential clinical significance in predicting platelet apoptosis in PTR patients.

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来源期刊
中国实验血液学杂志
中国实验血液学杂志 Medicine-Medicine (all)
CiteScore
0.40
自引率
0.00%
发文量
7331
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