Correction
for Newburg et al., Glycobiology 14 (3) 253-263.
Glycobiology vol 14 no 5 pp. 13G, 2004
Glycobiology vol. 14 no. 5 © Oxford University Press 2004; all rights reserved.
Erratum
In the article "Innate protection conferred by fucosylated oligosaccharides
of human milk against diarrhea in breastfed infants" by D.S.
Newburg, G.M. Ruiz-Palacios, M. Altaye, P. Chaturvedi, J. Meinzen-Derr,
M. de Lourdes Guerrero, and A.L. Morrow (
Glycobiology volume
14 number 3, pages 253–263), the relationship between
the observed maternal Lewis blood group phenotypes (
Table III)
and inferred maternal genotypes (
Table II) was inadvertently
omitted during publication. The Hardy-Weinberg distribution
of Lewis and secretor genotypes (
Table II) is based on assumed
gene frequencies whose validity is supported by the concordance
of expected with observed phenotype in
Table III. The shading
in
Tables II and
III indicates that each Lewis blood phenotype
represents multiple, but related, genotypes. Mothers of the
Lewis a–b– serological phenotype are of the genotype
lele (homozygous recessive for the Lewis gene, or
FUT 3), irrespective
of their secretor (Se, or
FUT 2) genotype (blue top rows,
Tables II and
III). The remaining mothers all have a dominant Lewis
gene (Lele or LeLe): Lewis a+b– phenotype, rare in this
population, is homozygous recessive for the secretor gene (sese)
(yellow left column,
Table II; yellow bottom row,
Table III),
while Lewis a–b+ phenotype, the most prevalent, has a
dominant secretor gene (Sese or SeSe) and Lewis gene (salmon
colored boxes,
Tables II and
III). A relationship between maternal
Lewis blood group phenotypes and patterns of fucosylated oligosaccharides
in their milk would support the premise that the polymorphisms
of these genes responsible for the Lewis blood group types also
underlie heterogeneous expression of milk fucosyloligosaccharides.
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