“…These data com plement those on the frequencies of secretors in Aborigines and Caucasians [12,21,22] which show that about 2% of Aborigines tested are non-secretors, in comparison with about 22% of Australian Caucasians [2].…”
Section: Discussionsupporting
confidence: 82%
“…This division is consistent with the expectation that O secretors have less Lea and more Leb than At secretors. Further, Vos and C omley [22] provide data (table II) showing that on red cells, those At cells with strong A expression have weaker Leb expression than cells with weak A expression.…”
Section: Discussionmentioning
confidence: 98%
“…Ulex europaeus (anti-H) and Dolichos biflorus (anti-A,) extracts, and anti-A and anti-B have been described elsewhere [2], Lewis groups of red cells of Aborigines were determined in the field, within 12 h of collection, using anti-Lea and anti-Leb antisera supplied by, and the technique of Vos [22], Anti-Lea used in agglutination inhibition studies was from an AB Le(a-b-) donor, lot 673-1, and was supplied by Dr. P. Stur geon.…”
Section: Methodsmentioning
confidence: 99%
“…However, exceptions have been noted. Recently reported exceptions include a Japanese family where the parents and one child are secretors of A but not H antigen, and whose red cells group as A1( Le(a + b + ) [ 14]; 11 out of 134 Thais who secrete A or B but not H antigens, and whose cells group as Le(a + b-) [6]; 16% of 355 Australian Aborigines who secrete A and/or H and whose red cells group as Le(a + ) [22], Further indications that an appreciable proportion of Australian Abori gines who are secretors (and most of them are) have red cells which react with anti-Lea, can be seen in the collection of reports of Lewis-typings of red cells, compared with the reports of the frequencies of non-secretors among Aborigines .compiled by Kirk [12]. Some series of tests have shown up to 10-15% of Le(a + ) Aborigines, whereas the frequency of non-secretors has been reported as being about 2% [12,21,22].…”
mentioning
confidence: 99%
“…Since Vos and Comley [22], who had, similarly, observed the Le(a + b + ) phenotype among Aboriginal secretors, proposed that the red cells of secretors gave some degree of Lea reaction because of the lower amount of H and the higher amount of Lea substances in the saliva of Aborigines, a comparative quantitative study of the ABO(H) and Lea substances in the salivas of Australian Aborigines and of Australian Caucasians was undertaken. The results of these studies are presented here.…”
Aboriginal secretors synthesize greater concentrations of H, A and Lea antigens than do Caucasians but, in Ax secretors, most H determinants are converted to A. Since Aboriginal secretors have concentrations of Lea in the saliva similar to those of Caucasian non-secretors, it is suggested that the red cell phenotype, Le(a+b+), observed in over 10% of Aborigines, is due to the high concentration of Lea which is not converted to Leb. Aboriginal A1secretors have significantly greater concentrations of Lea in their salivas than have·secretors. This observation has led to the proposal that, in the genetically-controlled biosynthetic pathways leading to the production of Lewis and ABH antigens in saliva, the genes add their specificities in the order H, A (and/or presumably B), Le.
“…These data com plement those on the frequencies of secretors in Aborigines and Caucasians [12,21,22] which show that about 2% of Aborigines tested are non-secretors, in comparison with about 22% of Australian Caucasians [2].…”
Section: Discussionsupporting
confidence: 82%
“…This division is consistent with the expectation that O secretors have less Lea and more Leb than At secretors. Further, Vos and C omley [22] provide data (table II) showing that on red cells, those At cells with strong A expression have weaker Leb expression than cells with weak A expression.…”
Section: Discussionmentioning
confidence: 98%
“…Ulex europaeus (anti-H) and Dolichos biflorus (anti-A,) extracts, and anti-A and anti-B have been described elsewhere [2], Lewis groups of red cells of Aborigines were determined in the field, within 12 h of collection, using anti-Lea and anti-Leb antisera supplied by, and the technique of Vos [22], Anti-Lea used in agglutination inhibition studies was from an AB Le(a-b-) donor, lot 673-1, and was supplied by Dr. P. Stur geon.…”
Section: Methodsmentioning
confidence: 99%
“…However, exceptions have been noted. Recently reported exceptions include a Japanese family where the parents and one child are secretors of A but not H antigen, and whose red cells group as A1( Le(a + b + ) [ 14]; 11 out of 134 Thais who secrete A or B but not H antigens, and whose cells group as Le(a + b-) [6]; 16% of 355 Australian Aborigines who secrete A and/or H and whose red cells group as Le(a + ) [22], Further indications that an appreciable proportion of Australian Abori gines who are secretors (and most of them are) have red cells which react with anti-Lea, can be seen in the collection of reports of Lewis-typings of red cells, compared with the reports of the frequencies of non-secretors among Aborigines .compiled by Kirk [12]. Some series of tests have shown up to 10-15% of Le(a + ) Aborigines, whereas the frequency of non-secretors has been reported as being about 2% [12,21,22].…”
mentioning
confidence: 99%
“…Since Vos and Comley [22], who had, similarly, observed the Le(a + b + ) phenotype among Aboriginal secretors, proposed that the red cells of secretors gave some degree of Lea reaction because of the lower amount of H and the higher amount of Lea substances in the saliva of Aborigines, a comparative quantitative study of the ABO(H) and Lea substances in the salivas of Australian Aborigines and of Australian Caucasians was undertaken. The results of these studies are presented here.…”
Aboriginal secretors synthesize greater concentrations of H, A and Lea antigens than do Caucasians but, in Ax secretors, most H determinants are converted to A. Since Aboriginal secretors have concentrations of Lea in the saliva similar to those of Caucasian non-secretors, it is suggested that the red cell phenotype, Le(a+b+), observed in over 10% of Aborigines, is due to the high concentration of Lea which is not converted to Leb. Aboriginal A1secretors have significantly greater concentrations of Lea in their salivas than have·secretors. This observation has led to the proposal that, in the genetically-controlled biosynthetic pathways leading to the production of Lewis and ABH antigens in saliva, the genes add their specificities in the order H, A (and/or presumably B), Le.
Red cell Lewis antigens are carried by glycosphingolipids passively absorbed from plasma. Plasma was collected from a spectrum of individuals with normal and unusual Lewis/secretor phenotypes in order to investigate the glycolipid basis for the unusual phenotypes. Samples were obtained from: a Le(a+b-) ABH nonsecretor who secreted Lewis substances; a Le(a+b-) partial secretor; Le(a+b+) partial secretors; Le(a+b+) secretors; and a full range of normal Lewis/secretor phenotypes as controls. The Le(a+b+) samples represented Polynesian, Asian and Réunion Island ethnic backgrounds. Nonacid glycolipids were prepared, separated by thin-layer chromatography, and then immunostained with potent monoclonal antibodies of known specificity. Despite different serological profiles of the Le(a+b-) and Le(a+b+) Polynesian samples, their plasma glycolipid expressions were very similar, with both Le(a) and Le(b) co-expressed. The copresence of Le(a) and Le(b) in Le(a+b+) samples is in marked contrast to Caucasians with normal Lewis phenotypes, who have predominantly either Le(a) or Le(b). These results suggest that there is a range of the secretor transferases in different individuals, possibly due to different penetrance or to several weak variants. We also show that Lewis epitopes on longer and/or more complex core chains appear to be predominant in the Polynesian Le(a+b+) samples. The formation of these extended glycolipids is compatible with the concept that in the presence of reduced secretor fucosyltransferase activity, increased elongation of the precursor chain occurs, which supports the postulate that fucosylation of the precursor prevents or at least markedly reduces chain elongation.
The SewA385T mutation of the FUT2 gene was found to correlate with both the erthrocyte Le(a + b+) and/or salivary ABH partial-secretor phenotypes of Polynesians. Constructs with FUT1 and FUT2 wild type genes, and the FUT2 SewA385T, seG428A and seC571T mutated alleles, were cloned into pcDNAI, and expressed in COS-7 cells. COS-7 cells transfected with the SewA385T allele had weak, but detectable, alpha(1,2)fucosyltransferase activity, with an acceptor substrate pattern similar to the wild type FUT2 gene. Comparative kinetic studies from cell extracts with mutated SewA385T and wild type FUT2 alleles gave similar Km values, but less enzyme activity was present in cells transfected with SewA385T (Vmax 230 pmol h-1 mg-1), as compared to those transfected with FUT2 (Vmax 1030 pmol h-1 mg-1), suggesting that the mutated enzyme is more unstable. These results confirm that the molecular basis for the erythrocyte Le(a + b+), and the associated ABH salivary partial-secretor phenotype, is an amino acid change of Ile129-->Phe in the secretor alpha(1,2)fucosyltransferase.
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