de Chaisemartin L, de la Taille V, Nicaise-Roland P, Malard L, Beuscart C, et al.
Blood •
Allergic transfusion reactions (ATR) are potentially lethal adverse events that occur in ∼0.3% to 6% of plasma or platelet transfusions. The main mechanism described is an immunoglobulin E (IgE)-mediated response to donor proteins, such as IgA and haptoglobin in deficient patients. Recently, in a nationwide retrospective observational study, we reported that group O recipients of group B or AB platelet concentrates or plasma were at significantly higher risk of severe ATR than recipients with other ABO combinations. Given the antigenic proximity between group B determinant and the galactose-α-1,3-galactose (α-Gal) epitope, we hypothesize a role for α-Gal IgE-mediated sensitization in these ATR. In this report, we investigated the presence of anti-α-Gal IgE in a cohort of 59 patients with severe ATR. We found that group O recipients of group B or AB blood components (plasma or platelet concentrates) were substantially more likely to exhibit high titers of group B cross-reactive anti-α-Gal IgE than other patients, supporting our hypothesis that α-Gal sensitization underlies these severe ATR. These findings suggest that α-Gal sensitization is an additional mechanism responsible for ATR in major ABO-incompatible transfusion and should be systematically explored in group O patients having received group B/AB plasma or platelets.
Christiane Y, Aghayan M, Emonard H, Lallemand A, Mahieu P, et al.
Placenta •
The galactose alpha 1-3 galactose (Gal alpha 1-3 Gal) residue is a carbohydrate widely distributed in many non-human mammals. Since Gal alpha 1-3 Gal residues are described on the cell surface of tumor cells, we have examined the possibility of their expression on human trophoblastic cells at different stages of placental implantation and in various pregnancy-associated conditions. Using immunohistochemical methods, Gal alpha 1-3 Gal was demonstrated on interstitial and vascular trophoblast during pregnancy. For villous trophoblast, the staining disappeared in second trimester pregnancies. The density of staining for Gal alpha 1-3 Gal was increased in highly invasive trophoblast (mole and choriocarcinoma) and decreased in poorly invasive specimens (spontaneous abortion, XO monosomia). No cells displaying Gal alpha 1-3 Gal at their surface were identified in some segments of spiral arteries from pre-eclamptic women. The anti-Gal antibody titer increased in the first trimester of pregnancy and in the sera of pre-eclamptic and eclamptic patients. These findings suggest that Gal alpha 1-3 Gal residues could be considered as markers for trophoblast invasive capacity and that the binding of maternal anti-Gal antibodies to the trophoblast could contribute to limit trophoblastic invasion and thus participate to the immunological control of implantation.
