A preliminary study on the mechanism of xenotransplantation-related coagulation dysfunction mediated by immune complexes - platelet FcγRⅡa (CD32a)
10.12464/j.issn.1674-7445.2026053
- VernacularTitle:免疫复合物-血小板FcγRⅡa（CD32a）介导的异种移植相关凝血功能障碍机制的初步研究
- Author:
Liqiang ZHAO
1
;
Quancheng WANG
1
;
Chuheng GOU
1
;
Hong ZHANG
1
;
Xin HONG
1
;
Xuan ZHANG
1
;
Kefeng DOU
1
Author Information
1. Department of Hepatobiliary Surgery, Xijing Hospital, Air Force Medical University, Xi'an 710032, China.
- Publication Type:OriginalArticle
- Keywords:
Xenotransplantation;
Coagulation dysfunction;
Platelet;
FcγRⅡa (CD32a);
Immune complex;
Porcine aortic endothelial cell;
Coagulation complication;
Shortage of donor organ
- From:
Organ Transplantation
2026;17(3):405-412
- CountryChina
- Language:Chinese
-
Abstract:
Objective To establish an "human serum - porcine aortic endothelial cells (PAEC) - human platelets" in vitro model and explore the mechanism of xenotransplantation-related coagulation dysfunction mediated by immune complexes - platelet FcγRⅡa (CD32a) receptor. Methods Healthy human serum was co-incubated with PAEC to prepare the supernatant containing immune complexes, which was then used to stimulate healthy human platelets, or directly treated with the serum of xenogeneic liver transplant recipients. Flow cytometry was used to detect platelet activation markers CD62P and surface IgG binding levels, and the platelet adhesion function was evaluated by platelet-PAEC adhesion experiments. CD32a blocking antibody IV.3 and SYK blocker SKYIN 4 were used to clarify the signaling pathways. Results The supernatant from the co-incubation of healthy human serum and PAEC could significantly induce platelet activation and endothelial adhesion. The use of the serum from xenogeneic liver transplant recipients could also significantly induce platelet activation. Antibody IV.3 and SYK blocker SKYIN 4 could significantly inhibit these effects. Conclusions In xenotransplantation, the immune complexes formed by human serum antibodies and porcine endothelial antigens may induce abnormal platelet activation through the platelet CD32a receptor, which is an important mechanism of non-complement-dependent post-transplant coagulation dysfunction, providing a new target for the intervention of coagulation complications in xenotransplantation.
