Quantitative Hemagglutination Inhibition Studies of Blood‐group Substances

Gibbs, Mary B.; Collins, William S.; Ortaldo, John R.; Laffer, C.

doi:10.1111/j.1537-2995.1971.tb04367.x

Cited by 2 publications

(1 citation statement)

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“…GIBBS et al [14] have demonstrated that a mixture of anti-A, A substance and A red cells resulted in a state of equilibrium between the three components since the strength of the agglutination was the same irrespective of the order in which the components were added. Thus, it would appear that the blood group substance exerts its main protective effect by competing with the red cells for available antibody and not by coating the sensitised cells as suggested by the studies of VOS and KIRK [44].…”

Section: Discussionmentioning

confidence: 99%

The Pathogenesis of ABO Haemolytic Disease of the Newborn

Voak

1969

Vox Sanguinis

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A study of the pathogenesis of ABO HD is essentially a study of the interrelationships of the maternal IgG anti-A/anti-B antibodies with the various components of the 'protective mechanism'.There is an equilibrium of IgG antibodies across the placenta and thus, ABO HD occurs more frequently in cases with high titre IgG antibodies than in cases with low titre IgG antibodies.The foetal blood group substance 'protects' the infants by competing with the red cells for the incompatible antibodies. Small amounts of the homologous blood group substance reduce the IgG anti-A/anti-B reaction with A/B red cells and the degree of inhibition increases as the antigenic strength of the red cells decreases.Possible reasons for the difference in combining power of the various adult and foetal red cells are discussed.A small deficiency of non-secretor infants and fathers was observed and the possible roles of secretor status in ABO HD are discussed.The incidence of A130 haemolytic disease (ABO HD) is far lower than the incidence of ABO incompatible pregnancies and it was realised t h a t this must result from the action of a protective mechanism. This was believed t o consist of, soluble A or B blood group substances in the foetus [l, 39,401, weak foetal antigens [22,40], and the restriction by the placental barrier on the passage of antibody from mother t o foetus. (Only 'complete' antibodies known at that time.) The protective mechanism was studied by TOVEY [40] and his paper should be consulted for a review of the early work.Soon after the demonstration of incomplete antibodies, WIENER and SONN [45] showed that the placenta was permeable t o the incomplete antibodies. I n a later paper WIENER and UNGER [47] demonstrated that the babies of group 0 mothers are apt to acquire about sixteen times as much antibody as babies with mothers of

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Section: Discussionmentioning

confidence: 99%