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[Acquired B antigen].

A Gerbal, C Ropars

    Revue Francaise De Transfusion Et Immuno-Hematologie
    |March 1, 1976
    PubMed
    Summary
    This summary is machine-generated.

    Acquired B antigen in group A individuals is linked to deacetylase enzymes, which alter the A specific sugar, N-acetylgalactosamine, causing cross-reactivity with anti-B sera. This phenomenon is associated with gastrointestinal disease and infectious syndromes.

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    Area of Science:

    • * Hematology: Focuses on blood group antigens and their serological properties.
    • * Biochemistry: Investigates enzymatic modifications of blood group specific sugars.

    Context:

    • * Acquired B antigen is typically observed in individuals with group A blood, often associated with digestive tract diseases like colon cancer.
    • * Previous studies indicated differences between acquired B antigen and normal B antigens, with group A1 cells showing altered reactivity.

    Purpose:

    • * To explore the biochemical basis of acquired B antigen formation in group A individuals.
    • * To investigate the role of deacetylase enzymes in the alteration of blood group A specificity.

    Summary:

    • * Acquired B antigen in group A1 individuals is linked to a deacetylase enzyme that modifies N-acetylgalactosamine (the A-specific sugar) into galactosamine, enabling cross-reactivity with anti-B sera.

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  • * This acquired B activity is associated with infectious syndromes and gastrointestinal diseases, and can be reversed by acetylation.
  • * A distinct polyagglutinability is also observed in acquired B cells, potentially due to deacetylation of N-acetyl-neuraminic acid.

    • Impact:

    • * Confirms the enzymatic basis of acquired B antigen, providing a deeper understanding of blood group antigen modifications.
    • * Highlights the clinical relevance of acquired B antigen in patients with gastrointestinal issues and infectious conditions.
    • * Offers insights into the mechanisms of polyagglutinability and its relationship with enzymatic alterations in red blood cells.