The Recognition of Water-Soluble I Blood Group Substance

Abstract

A powerful cold auto anti-I has been found that is strongly inhibited by hydatid cyst fluid and inhibited to a varying extent by all of the 181 human saliva samples tested. The investigation showed that the inhibition effect was specific for I and that water soluble I blood group substance must be responsible. No correlation could be found between the concentration of I substance in the saliva and the presence of ABH, Lewis or Sda substances. The amount of salivary I substance secreted appears to be a constant feature of the individual. Infants at birth and i adults have high concentrations of I substance in their saliva and the amount of I substance present does not reflect the I status of the red cells.

Molecular basis of the adult i phenotype and the gene responsible for the expression of the human blood group I antigen

“…Synthesis of I antigens in different tissues has been suggested to result from different I-branching enzymes given that normal quantities of I antigen in saliva, milk, and plasma of persons with adult i phenotype has been observed. 37,38 A similar situation has been demonstrated in the formation of blood group H antigens in RBC membrane and in saliva, which are synthesized by the action of different ␣-1,2-fucosyltransferases encoded by the H and Secretor genes, respectively. 39 Whether the other I-branching enzyme encoding gene, C2GnT-M, or another unidentified gene is responsible for the I antigen expression in secretions remains to be determined.…”

A novel I-branching β-1,6-N-acetylglucosaminyltransferase involved in human blood group I antigen expression

“…On the other hand, healthy quantities of I antigen have been detected in saliva, milk, and plasma of persons with the adult i phenotype of erythrocytes. 15,16 The discrepancy between blood type i and histo-blood group I antigens might have resulted from novel IGnTs, which have not cloned yet, showing a different profile of tissue distribution from conventional IGnT1. According to our own experiments of the transcript expression and the previous experimental data on the BAC clones, it is considered that 3 IGnTs are generated by alternative splicing of a single gene, sharing exons 2 and 3, which was mapped at major blood group I locus on chromosome 6.…”

“…Moreover, it is suggested that the discrepancy between blood group and histo-blood group I/i antigen expression can be explained by differential gene regulation of IGnT3 and the other IGnTs and C2GnT-2. 11,12,15,16 Although such gene regulation mechanism has not been examined in humans, it is noteworthy that remarkable IGnT3 gene expression is induced during erythroid differentiation of CD34 ϩ cells. The regulatory region of human IGnT3 may be different from those of IGnT1 and IGnT2 and would be in the downstream of erythropoietin signal transduction.…”

“…It is of interest that the water-soluble I blood group substance was detected in white i adults. 15,16 In addition, it was reported that the adult i phenotype in Japanese persons is often associated with congenital cataracts. 33 The i blood type of individuals in the present study is associated with cataracts, as described in "Materials and methods."…”

“…In previous studies, healthy quantities of I antigen have been detected in saliva, milk, and plasma of an individual with the adult i phenotype of erythrocytes. 15,16 These findings suggest that there may be additional IGnT genes responsible for histo-blood group I antigen, and the elucidation of the genes should contribute to a better understanding of the blood group I gene locus.…”