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    Home > Active Ingredient News > Blood System > Transfusion: Autoantibodies against glycoprotein A on the surface of red blood cells affect the activation state of circulating white blood cells

    Transfusion: Autoantibodies against glycoprotein A on the surface of red blood cells affect the activation state of circulating white blood cells

    • Last Update: 2021-12-01
    • Source: Internet
    • Author: User
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    Both the M and N alleles encode an antigen on glycoprotein A (GPA), which is a red blood cell (RBC) surface sialoglycoprotein
    .
    The interaction between RBC GPA and leukocyte surface lectins may down-regulate their activation
    .
    The current study investigated whether RBC's autoantibodies against GPA, such as autoanti-M/N, can trigger an activated phenotype in peripheral blood leukocytes
    .

    Both the M and N alleles encode an antigen on glycoprotein A (GPA), which is a red blood cell (RBC) surface sialoglycoprotein
    .
    The interaction between RBC GPA and leukocyte surface lectins may down-regulate their activation
    .
    The current study investigated whether RBC's autoantibodies against GPA, such as autoanti-M/N, can trigger an activated phenotype in peripheral blood leukocytes
    .

    Leukocyte activation was evaluated in whole blood from patients with autoanti-GPA (anti-M/N) and compared with patients with allogeneic anti-M/N and healthy subjects


    .
    Analysis of control samples from healthy subjects without antibodies incubated with anti-GPA or anti-Rh in vitro to determine the expression of neutrophil and monocyte surface activation markers, the content of reactive oxygen species (ROS), and the interaction with RBC The formation of aggregates


    Leukocyte activation was evaluated in whole blood from patients with autoanti-GPA (anti-M/N) and compared with patients with allogeneic anti-M/N and healthy subjects
    .
    Analysis of control samples from healthy subjects without antibodies incubated with anti-GPA or anti-Rh in vitro to determine the expression of neutrophil and monocyte surface activation markers, the content of reactive oxygen species (ROS), and the interaction with RBC The formation of aggregates


    Table 1: Characteristics of patients with autologous anti-M or allogeneic anti-M/N antibodies Table 1: Characteristics of patients with autologous anti-M or allogeneic anti-M/N antibodies

    Table 2: Complete blood count (mean ± standard deviation)

    Table 2: Complete blood count (mean ± standard deviation) Table 2: Complete blood count (mean ± standard deviation)

    Figure 1: In vivo and in vitro expression of leukocyte surface activation markers

    Figure 1: In vivo and in vitro expression of leukocyte surface activation markers Figure 1: In vivo and in vitro expression of leukocyte surface activation markers

    Figure 2: In vitro detection of white blood cells and intracellular ROS content

    Figure 2: In vitro detection of white blood cell and intracellular ROS content Figure 2: In vitro detection of white blood cell and intracellular ROS content

     

    Figure 3: Neutrophil-erythrocyte aggregation in vitro

    Figure 3: Neutrophil-erythrocyte aggregation in vitro Figure 3: Neutrophil-erythrocyte aggregation in vitro

    Patients with allogeneic anti-M/N (p = .


    Patients with allogeneic anti-M/N (p = .


    In summary, exposure of neutrophils and monocytes in peripheral blood to antibodies against GPA on the RBC surface, such as M or N antigens, may trigger an activated phenotype


    In summary, exposure of neutrophils and monocytes in peripheral blood to antibodies against GPA on the RBC surface, such as M or N antigens, may trigger an activated phenotype


    Original source:

    Klein, MN ,  Larkin, EJ ,  Marshall, JN ,  Fan, X ,  Parry, P ,  Tirouvanziam, R , et al.


    Klein, MN ,  Larkin, EJ ,  Marshall, JN ,  Fan, X ,  Parry, P ,  Tirouvanziam, R , et al.
      Autoantibodies to red blood cell surface Glycophorin A impact the activation poise of circulating leukocytes .
      Transfusion .
      2021 ;  1 –  10 .
      https://doi.
    org/10.
    1111/trf.
    16746

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