Objectives: To explore the relationships between the peripheral blood levels of CD61, CD63, PAC-1 and the incidence of acute rejection and tubular necrosis after renal transplantation, and recovery of the graft function.
Methods: The peripheral blood levels of CD61, CD63, and PAC-1 of 86 patients with uremia in different stages before and after transplantations were analyzed by flow cytometry. The patients were divided into three groups: (1) twenty-nine patients with normal grafts function, (2) hirty with acute rejection and (3) twenty-seven with acute tubular necrosis. The patients with acute rejection were randomly divided into treatment group with anticoagulants and cntrol group.
Results: The peripheral blood levels of CD61, CD63 and PAC-1 significantly increased (P < 0.05) in the patients with acute rejection, in comparison with those with normal grafts function and those with acute tubular necrosis. The peripheral blood levels of CD61, CD63 and PAC-1 in patients with acute rejection in anticoagulants therapy was lower, recovery time of the grafts function was shorter, one-year survival rates of patients and grafts were higher, as compared with those of controls.
Conclusions: The patients with acute rejection have significantly high peripheral blood levels of CD61, CD63 and PAC-1 before transplantation, however, these values in patients with acute tubular necrosis are not high, this suggesting that acute rejection might relate to platelet activation, while acute tubular necrosis might not relate to it. After anticoagulants therapy in patients with acute rejection, the grafts function might recover faster and their one-year survival rates and grafts might be higher in those with CD61, CD63 and PAC-1 decreasing remarkably.
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Int J Mol Sci
January 2025
Immunology Department, University Hospital Marqués de Valdecilla, 39008 Santander, Spain.
The human leukocyte antigen (HLA) system plays a critical role in transplant immunology, influencing outcomes through various immune-mediated rejection mechanisms. Hyperacute rejection is driven by preformed donor-specific antibodies (DSAs) targeting HLAs, leading to complement activation and graft loss within hours to days. Acute rejection typically occurs within six months post-transplantation, involving cellular and humoral responses, including the formation of de novo DSAs.
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State Key Laboratory of Experimental Hematology, National Clinical Research Center for Blood Diseases, Haihe Laboratory of Cell Ecosystem, Institute of Hematology & Blood Diseases Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin, 300020, China.
Background: The benefit of universal CAR-T cells over autologous CAR-T cell therapy is that they are a treatment that is ready to use. However, the prevention of graft-versus-host disease (GVHD) and host-versus-graft reaction (HVGR) remains challenging. Deleting class I of human leukocyte antigen (HLA-I) and class II of human leukocyte antigen (HLA-II) can prevent rejection by allogeneic T cells; however, natural killer (NK) cell rejection due to the loss of self-recognition remains unresolved.
View Article and Find Full Text PDFPLoS One
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Transplant Group, La Paz University Hospital Health Research Institute (IdiPAZ), Madrid, Spain.
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Department of General Surgery, Tianjin Medical University General Hospital, No. 154, Anshan Road, Heping District, Tianjin, 300052, China.
Background: Acute rejection (AR) is one of the significant factors contributing to poor prognosis in patients following kidney transplantation. Neutrophils are the main cause of early host-induced tissue injury. This paper intends to investigate the possible mechanisms of neutrophil involvement in acute rejection in renal transplantation.
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