Analysis of Correlation between Platelet Desialylation, Apoptosis and Platelet Alloantibody and CD8+ T Cells in Platelet Transfusion Refractoriness.
10.19746/j.cnki.issn.1009-2137.2025.04.031
- Author:
Yan ZHOU
1
;
Li-Yang LIANG
1
;
Chang-Shan SU
1
;
Hui-Hui MO
1
;
Ying CHEN
1
;
Fang LU
1
;
Yu-Chen HUANG
1
;
Zhou-Lin ZHONG
1
Author Information
1. Nanning Blood Center (Nanning Institute of Transfusion Medicine), Nanning 530007, Guangxi Zhuang Autonomous Region, China.
- Publication Type:Journal Article
- Keywords:
PTR;
desialylation;
apoptosis;
alloantibody;
CD8
- MeSH:
Humans;
Apoptosis;
CD8-Positive T-Lymphocytes/immunology*;
Blood Platelets/metabolism*;
Platelet Transfusion;
Isoantibodies;
Male;
Female;
Middle Aged
- From:
Journal of Experimental Hematology
2025;33(4):1138-1144
- CountryChina
- Language:Chinese
-
Abstract:
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 vitro （P < 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.
