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#cell surface markers

2 public questions tagged with this topic.

Glycolipid and Phospholipid

Which of the following plays a role in blood group antigen formation?

Glycosylation modifications influence ABO antigen presentation beyond core transferase reactions involving fucose GalNAc Gal additions to H substance. Sialic acid N acetylneuraminic acid added ST3GAL ST6GAL1 sialyltransferases using CMP Neu5Ac caps galactose residues precursor polylactosamine chains via alpha two three alpha two six linkages introducing negative charge repelling pathogens masking H antigen lectin binding modulating accessibility and complement regulation. On erythrocyte membrane glycophorin A carries fifteen O linked one N linked sialylated tetrasaccharides accounting major negative zeta potential minus fifteen millivolts reducing aggregation controlling alternative complement via factor H binding sialic acid polyanion host marker. ABO antigens reside same polylactosamine carriers sialylation status regulates accessibility terminal GalNAc Gal anti A anti B IgM agglutination and lectin Dolichos biflorus DBA. Sialic acid also serves receptor influenza hemagglutinin Plasmodium EBA175 invasion. Phosphatidylinositol triacylglycerol ergosterol do not contribute extracellular glycan epitopes blood group serology. Thus sialic acid role modulator antigen formation red cell surface properties exemplifies glycobiology intersection transfusion science infectious disease susceptibility immune evasion mechanisms tested serology exams and immunohematology contexts and ABO discrepancies.

Ref: Varki A., Glycobiology 2008, Sialic acids blood group antigen modulation masking and recognition.

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Glycolipid and Phospholipid

Which statement is true about ABO blood group antigens?

ABO antigens represent terminal glycosylation differences on H precursor anchored glycolipid or glycoprotein paragloboside type two chain precursor. H synthesis requires FUT1 alpha one two fucosyltransferase attaching fucose galactose beta1-4 GlcNAc forming Fuc alpha1-2 Gal structure. Functional A allele encodes alpha one three N acetylgalactosaminyltransferase GTA adding GalNAc galactose H forming A trisaccharide GalNAc alpha1-3(Fuc alpha1-2)Gal antigen A. B allele encodes alpha one three galactosyltransferase GTB adding galactose forming B trisaccharide Gal alpha1-3(Fuc alpha1-2)Gal antigen B. O allele harbors two six one delG frameshift producing truncated soluble inactive enzyme lacking catalytic domain so H remains unconverted due absent transferase activity producing O phenotype H antigen only. O individuals therefore lack A B glycosyltransferases but retain FUT1 FUT2 fucosyltransferases required Bombay phenotype hh. Misstatements Type A adding galactose or Type B lacking modification incorrect. Genetics explains transfusion reactions anti A anti B IgM natural antibodies isoagglutinins and Bombay phenotype hh lacking fucosyltransferase producing no H substrate requiring Bombay blood donations extremely rare compatible blood type cases.

Ref: Yamamoto F., Transfusion Med Rev 2004, ABO genetics O inactivity transferase and H antigen.

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