Expression of ABH and X (Lex) antigens on platelets and lymphocytes

Abstract

We used a panel of reagents, polyclonal and monoclonal antibodies, and lectins to define the expression of the ABH- and Lewis-related specificities on platelets and lymphocytes. We also determined the expression of the alpha 2- and alpha 3-L-fucosyltransferases necessary for their biosynthesis. The antigens that could be detected by immunofluorescence and Western blot analysis were based on type 2 monofucosylated structures. Antibodies directed toward types 1, 3, and 4 ABH-, X- and Lewis-related antigenic determinants were always negative because the small amounts of ABH and Lewis antigens adsorbed from the serum could not be detected by these techniques. The presence of the type 2 ABH antigens on intrinsic glycoproteins was controlled by the H gene. This correlates with the presence of alpha 2-L- fucosyltransferase and the absence of alpha 3-L-fucosyltransferase on platelets. In contrast, ABH antigens were not detected by immunofluorescence on normal peripheral lymphocytes. These cells thus have only the small amounts of antigens adsorbed from the serum, these being under control of the secretor and Lewis genes. This correlates with the absence of alpha 2-L-fucosyltransferase on lymphocytes. When lymphocytes were transformed in vitro by the Epstein-Barr virus (EBV), however, they strongly expressed the X and sialylated X antigens, which are specific markers of normal granulocytes and monocytes, respectively. Treatment of EBV-transformed lymphoblastoid cell lines with 12-O-tetradecanoylphorbol-13-O-acetate significantly decreased the expression of X and sialylated X antigens along with that of surface immunoglobulins, whereas it induced a significant expression of the H antigen under control of the H gene.

The Novel Coronavirus SARS-CoV-2 Vulnerability Association with ABO/Rh Blood Types

“…RH blood grouping categorizes in two phenotypes D+ and D-depending on the presence or absence of D protein epitopes (16)(17)(18). ABO histo-blood group antigens have been found in RBC's surface lymphocytes, as well as many tissue organs, mucosal surfaces, and exocrine secretions (13,(19)(20)(21)(22)(23). The human body produces antibodies against the missing ABO histo-blood group antigens resulting in the production of anti-A and/or anti-B antibodies (13,24).…”

Blood group A antigen expression in platelets is prominently associated with glycoprotein Ib and IIb. Evidence for an A1/A2 difference

“…Also, by immunofluorescence, the IgG antibodies from individuals with high anti-A titres have been shown to react with blood group A 1 but not A 2 platelets (Skogen et al, 1988). Furthermore, it was found that an anti-A antibody strongly stained bands around 140-130 kDa under reducing conditions; weaker bands ranging between 160 and 60 kDa were also labelled (Mollicone et al, 1988). These investigators suggested that the major band could correspond to GPIb, but it was not further characterized.…”

“…The intrinsic determinants have been considered to be associated with glycolipids rather than glycoproteins (Dunstan & Mansbach, 1985). Never-theless, in two recent reports anti-A antibodies were found to react with platelet glycoproteins with an approximate molecular weight of 130-140 kDa but not further characterized (Mollicone et al, 1988;Holgersson et al, 1990). In another study, blood group A determinants were assigned to GPIb, IIa and IIIa (Santoso et al, 1991).…”

Blood Groups in Infection and Host Susceptibility

“…ABH-active gp120 can be produced in vitro by propagating HIV in cell lines expressing the appropriate glycosyltransferases (280). ABH-active HIV can also be produced by propagating HIV in lymphocytes of a known ABO type (280,281), despite the reported absence of ABH on lymphocyte glycoproteins (282). However, lymphocytes adsorb ABH-active GSLs from plasma (283).…”