The identification of antibodies to platelet-specific antigens is important for correctly diagnosing neonatal alloimmune thrombocytopenia, posttransfusion purpura and refractoriness due to platelet-specific antibodies. However, the serologic identification of these platelet-specific antibodies is complicated by the presence of anti-HLA antibodies. We examined and compared the diagnostic usefulness of acid-treated and chloroquine-treated platelets for the discrimination of platelet-specific antibodies from anti-HLA antibodies. The viability of acid-treated platelets is 83.4%, which is better than that of chloroquine-treated platelets (52.6%). The antigenicity of HLA class I antigens of acid-treated platelets was significantly reduced compared with that of PBS- or chloroquine-treated platelets. On the other hand, platelet surface glycoprotein Ib and glycoprotein IIb/IIIa, and platelet-specific antigens were stable following acid or chloroquine treatment. Chloroquine-treated platelets were not suitable targets for analysis by immunofluorescence flow cytometry because of nonspecific fluorescence derived from platelet damage. We conclude that acid-treated platelets are more suitable targets than chloroquine-treated platelets for screening for platelet-specific antibodies and also for analyses of the specificity of platelet-specific antibodies.

Download full-text PDF

Source
http://dx.doi.org/10.1111/j.1423-0410.1990.tb05020.xDOI Listing

Publication Analysis

Top Keywords

platelet-specific antibodies
24
chloroquine-treated platelets
20
anti-hla antibodies
12
acid-treated platelets
12
antibodies
10
platelets
9
platelet-specific
8
antibodies anti-hla
8
chloroquine treatment
8
platelet-specific antigens
8

Similar Publications

Human platelet antigens (HPAs) play a clinically significant role in alloimmunization and the development of immune-mediated disorders such as immune thrombocytopenia (ITP), fetal and neonatal alloimmune thrombocytopenia (FNAIT), and post-transfusion purpura (PTP). Understanding the genetic profiles of HPAs is critical for preventing and treating these conditions. Given the limitations of serological methods in determining HPA genotypes, this study aims to investigate the association between the genotypes of HPA1, HPA2, HPA3, HPA4, and HPA15 antigens and autoimmune thrombocytopenia in Lorestan Province, utilizing the PCR-SSP method.

View Article and Find Full Text PDF

Autoimmune effector mechanisms associated with a defective immunosuppressive axis in immune thrombocytopenia (ITP).

Autoimmun Rev

December 2024

Division of Hematology and Transfusion Medicine, Lund University, Lund, Sweden; Clinical Immunology and Transfusion Medicine, Office of Medical Services, Region Skåne, Lund, Sweden; Departments of Pharmacology, Medicine and Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Canada. Electronic address:

Article Synopsis
  • Immune thrombocytopenia (ITP) is an autoimmune disorder marked by low platelet counts, with varying symptoms ranging from no bleeding to severe, potentially fatal bleeding.
  • The disease involves a malfunction in the immune system, particularly a hyperactive response from certain immune cells that destroy platelets and their precursors.
  • Key factors in this condition include a breakdown of immune regulation, characterized by defects in certain immunosuppressive cells, leading to an uncontrolled immune response that attacks platelets and disrupts their production.
View Article and Find Full Text PDF

Functional characterization of a nanobody-based glycoprotein VI-specific platelet agonist.

Res Pract Thromb Haemost

October 2024

Center for Benign Haematology, Thrombosis and Haemostasis, Van Creveldkliniek, University Medical Center Utrecht, Utrecht University, Utrecht, the Netherlands.

Background: Glycoprotein (GP)VI is a platelet-specific collagen receptor required for platelet activation during hemostasis. Platelet reactivity toward collagen is routinely assessed during diagnostic workup of platelet disorders. GPVI can be activated by inducing receptor clustering with suspensions of fibrillar collagen or synthetic cross-linked collagen-related peptide (CRP-XL).

View Article and Find Full Text PDF

[Platelet-specific knockout inhibits platelet production and activation and reduces thrombosis in mice].

Nan Fang Yi Ke Da Xue Xue Bao

August 2024

Department of Biochemistry and Molecular Biology, Southern Medical University, Guangzhou 510515, China.

Objective: To investigate the effects of platelet-specific knockout on platelet activation and thrombus formation in mice.

Methods: PF4-Cre and Rictor transgenic mice were crossed to obtain platelet-specific knockout (-KO) mice and wild-type mice (=65), whose expression levels of Rictor, protein kinase B (AKT) and p-AKT were detected using Western blotting. Platelet counts of the mice were determined using routine blood tests, and hemostatic function was assessed by tail vein hemorrhage test.

View Article and Find Full Text PDF
Article Synopsis
  • - Platelets show immune responsiveness in various diseases, like sepsis and COVID-19, and play a role in the immune response to malaria caused by the Plasmodium parasite, specifically evidenced by changes in messenger RNA in infected mice.
  • - In a study with non-lethal Plasmodium yoelii-infected mice, platelet Ido1 expression increased due to interferon-γ (IFN-γ), a cytokine that enhances this enzyme, leading to higher kynurenine levels and lower serotonin.
  • - Platelet-specific Ido1 knockout mice experienced higher mortality and lung thrombi during infection, suggesting that platelet Ido1 is crucial for managing immune responses and maintaining vascular stability after malaria infection.
View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!