Serum from a pregnant woman with the May-Hegglin anomaly contained a platelet-specific antibody. The serum reacted in the platelet indirect immunofluorescence test (PIIFT) with 97.6% of random donor platelets and those of the father but not with the mother's own platelets. This antibody induced a moderate thrombocytopenia in the infant that responded to infusion of intravenous immunoglobulin concentrates. The platelet phenotypes were PLA1+, Baka+, Bra+/Brb- for the mother, PLA1+, Baka+, Bra-/Brb+ for the father, and PLA1+, Bra+/Brb+ for the neonate. Analysis of the maternal serum with an immunoassay based on monoclonal antibody immobilization of platelet antigens (MAIPA) and immunoprecipitation techniques demonstrated the absence of antibodies directed against HLA class I antigens and that the antigen recognized was located on the platelet-GpIa/IIa complex. This antigen was present on 113/115 random donor platelets, in 7 of the 7 unrelated May-Hegglin platelets, and only absent in 3/24 Bra+ individuals, including the mother. No platelet-specific antibody was present in the serum of the 7 unrelated May-Hegglin subjects. The antigen recognized by this platelet-specific antibody thus meets the criteria defining the antithetic allele of Bra, i.e. the Brb alloantigen.

Download full-text PDF

Source
http://dx.doi.org/10.1111/j.1423-0410.1991.tb00911.xDOI Listing

Publication Analysis

Top Keywords

platelet-specific antibody
12
antibody serum
8
random donor
8
donor platelets
8
pla1+ baka+
8
antigen recognized
8
unrelated may-hegglin
8
antibody
5
brb platelet
4
platelet alloantigen
4

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!