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Rh antigen immunoreactivity after histidine modification.

E J Victoria, M J Branks, S P Masouredis

    Molecular Immunology
    |October 1, 1986
    PubMed
    Summary
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    Histidine modification of red blood cells (RBC) using chemical reagents like DEP and pBPB, and Rose Bengal photo-oxidation, impacts Rh antigen expression. These findings support histidine's role in Rh antigen activity.

    Area of Science:

    • Immunology
    • Biochemistry
    • Hematology

    Background:

    • Red blood cell (RBC) surface antigens, particularly Rh antigens, are crucial for blood transfusion compatibility.
    • Previous studies suggest a role for histidine residues in the expression or function of Rh antigens.

    Purpose of the Study:

    • To investigate the involvement of histidine in the expression of Rh antigens on red blood cells.
    • To determine if selective modification of histidine residues affects antibody binding to Rh antigens.

    Main Methods:

    • Red blood cells were treated with chemical reagents (diethylpyrocarbonate, p-bromophenacyl bromide) and Rose Bengal photo-oxidation to modify histidine residues.
    • Antibody binding assays using 125I-anti-D IgG and 125I-protein A were performed to assess the impact on Rh antigen expression.

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  • Serological reagents were used to confirm antigen inactivation.

    • Main Results:

    • Diethylpyrocarbonate (DEP) caused progressive inactivation of the D antigen.
    • p-bromophenacyl bromide (pBPB) treatment reduced 125I-anti-D IgG binding by 50%.
    • Rose Bengal (RB) photo-oxidation inactivated major Rh antigens (D, C, c, e) while leaving other blood group antigens (Fya, Fyb) unaffected.

    Conclusions:

    • The results strongly support the hypothesis that histidine residues are involved in Rh antigen activity.
    • Histidine may play a direct role in the epitope structure or indirectly modulate antigen expression at the lipid-protein interface.
    • Further research is needed to elucidate the precise mechanism of histidine involvement in Rh antigen expression.