F. Nakashima

The Lewis histo-blood group system is characterized by the expression of the Lea and Leb antigens in the gastrointestinal tract, whose synthesis results in interactions between α2-L-fucosyltransferase (FUTII) and α3/4-L-fucosyltransferase (FUTIII) enzymes coded by the FUT2 (19q.13.3) and FUT3 (19p13.3) genes. FUTII and FUTIII fucosylate the type 1 oligosaccharide precursor (Galβ1→3NAcGlcβ1→3-R) at distinct positions to form H type 1 (Fucα1→2Galβ1→3NAcGlcβ1→3-R) and Lea (Galβ1→3[Fucα1→4]NAcGlcβ1→3-R) antigens, respectively. The fucosylation of H type 1 antigens by FUTIII results in the Leb antigen (Fucα1→2Galβ1→3[Fucα1→4]NAcGlcβ1→3-R). Thus, the presence of the FUTII and FUTIII enzymes leads to the expression of the Le(a+b+) phenotype, while the presence of only FUTIII allows the expression of the Le(a+b-) phenotype. The absence of the FUTIII enzyme leads to the expression of the Le(a-b-) phenotype, independent of the presence or absence of FUTII. Point mutations in FUT2 and FUT3 genes change the activity of these enzymes, impair the synthesis of Lea and Leb antigens, and contribute to the variability of Lewis phenotypes in the gastrointestinal tract. Toxoplasma gondii, an apicomplexan parasite that infects a large proportion of the world’s population, utilizes the gastrointestinal tract as an infection route and seems to adhere to glycosylated molecules to invade human cells

Key words: Toxoplasmosis; FUT2; FUT3; Toxoplasma gondii; High-risk pregnancy; Lewis histo-blood group system