Detection and Characterization of Lewis Antigens in Plasma of Lewis‐Negative Individuals Evidence of Chain Extension as a Result of Reduced Fucosyltransferase Competition

Abstract

Nonacid plasma glycolipids from Lewis-negative individuals of nonsecretor, partial-secretor and secretor phenotypes were prepared and separated by thin-layer chromatography and immunostained with radiolabelled Lewis antibodies. Lewis-positive plasma and intestinal epithelial cell glycolipids from Caucasians representing the four recognized Lewis and secretor combined phenotypes were used as controls. By presenting these purified total glycolipids in a cell-free environment to Lewis antibodies we were able to demonstrate the presence of small amounts of Lewis antigens in Lewis-negative individuals. It is shown that lactotetraosylceramide and extended precursor glycolipids are present in all Le(a-b-) nonsecretors. Le(a) was detected in 1 of the 3 Le(a-b-) nonsecretor plasmas and in the intestinal sample of the same phenotype. Lactotetraosylceramide was absent but H type 1 and Le(b) were both present in all group O Le(a-b-) secretors, and extended H type 1 reactive structures were also found in the partial secretor. These results clearly demonstrate that although the Lewis-negative phenotype exists at the serological level, this phenotype is not an 'all-or-nothing' phenomenon at the chemical level. We also show that in the presence of reduced fucosyltransferase activity, increased elongation of the precursor chain occurs, which allows us to postulate that fucosylation of the precursor prevents or at least markedly reduces chain elongation.

Lewis and Secretor Gene Effects on Lewis Antigen and Postnatal Development of Lewis Blood Type

“…Evidence of Le a and Le b antigens in plasma of Le(ab-) individuals has already been reported by Henry et al [23]. In our experiment, the levels of Lewis antigens in plasma and bloodstains of Le(a-b-) blood type were due to the high detectability of our time-resolved fluoroimmunoassay using a new europium chelate as a label.…”

A Second Nonsecretor Allele of the Blood Group a(1,2)Fucosyltransferase Gene (FUT2)

“…These samples have been extensively Lewis and secretory phenotyped and in some instances glycolipids were immunochemically profiled [12][13][14][15], Lewis phenotypes reported are those based on red cell serol ogy; however, for 3 samples, the Le(a+b-) phenotype was not support ed by glycolipid analysis of plasma [15, unpubl. obs.]. These 3 samples (033, 057 and 114) arc examples of the Le(a+b+) phenotype in which the Leb reaction on red cells cannot be serologically demonstrated rou tinely, and these samples have been classified here as Le(a+b+).…”

DNA Sequencing and Screening for Point Mutations in the Human Lewis (FUT3) Gene Enables Molecular Genotyping of the Human Lewis Blood Group System

“…The latter condition is uncommon among whites (5-10% in Caucasian populations) but up to 5 times more common among black people [8]. The Lewis negativity, Le(a-b-), refers strictly to the serological reac tions of erythrocytes, since Lea or Leb antigens may be found in Lewis-negative individuals either in serum, plasma [9,10], saliva [11,12], on uroepithelial cells, or in colonic intestinal tissues [13], Until recently the allelic representation of Lewis blood group status was described as LeLe or Lele for Lewis-posi tive and lele for Lewis-negative individuals [8]. However, the cloning by Kukowska-Latallo et al [14] of the human Lewis a( 1,3/1,4)-fucosyltransferase [15,16] has opened up a new chapter for allelic characterisation and genotyping of human individuals for the Lewis blood group system.…”