A SLC14A1 c.230G>A variant causes loss of Kidd antigen expression

Background The Kidd (Jk) blood group system is defined by the Jk a , Jk b and Jk3 antigens encoded by the SLC14A1 gene. The Jk(a-b-) phenotype, characterized by the absence of these antigens, is a rare blood group phenotype with a low population frequency, and its molecular basis is primarily associated with variants in the SLC14A1 gene. Herein, we identified an individual with the Jk(a-b-) phenotype carrying a variant, and evaluated whether this variant affects Jk antigen expression. Methods The Jk(a-b-) phenotype was identified by conventional serological typing. The coding sequence of the SLC14A1 gene was analyzed using polymerase chain reaction sequence-based typing (PCR-SBT), and haplotype analysis was performed using single-molecule sequencing. The functional impact of the variant was evaluated through in vitro transfection and expression assays, and Jk b antigen expression on transfected cells was assessed by flow cytometry. The potential functional impact of the variant was also evaluated using in silico prediction tools. Results Jk a , Jk b and Jk3 antigens were absent in the proband. PCR-SBT identified three heterozygous single-nucleotide variants (SNVs) and two homozygous SNVs across four exons of the SLC14A1 gene. Single-molecule sequencing revealed two haplotypes: one comprising c.342-1G>A, c.588A>G, and c.838G>A, and the other comprising c.230G>A, c.499A>G, c.588A>G, and c.838G>A. In silico analysis predicted c.230G>A to be a deleterious variant and indicated that it altered interactions with neighboring atoms. Functional assays showed that cells transfected with JK(c.230G>A+c.499A>G+c.588A>G+c.838G>A) did not express the Jk b antigen, while cells transfected with the JK*02 allele or JK(c.499A>G+c.588A>G+c.838G>A) exhibited high levels of Jk b antigen expression. Conclusions A JK null allele and its critical SNV were identified, and the functional effect of the variant was confirmed through transfection and expression studies.

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Journal
Frontiers in Immunology
Published
2026-10-29
DOI
https://doi.org/10.3389/fimmu.2026.1922509
Primary Topic
Blood groups and transfusion
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article
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article

A SLC14A1 c.230G>A variant causes loss of Kidd antigen expression

Xiaozhen Hong, Jingjing Zhang, Yanling Ying, Faming Zhu et al.
2 links
Frontiers in Immunology
Blood groups and transfusion
article

A SLC14A1 c.230G>A variant causes loss of Kidd antigen expression

Xiaozhen Hong, Jingjing Zhang, Yanling Ying, Faming Zhu, Xianguo Xu
article en

Abstract

Background The Kidd (Jk) blood group system is defined by the Jk a , Jk b and Jk3 antigens encoded by the SLC14A1 gene. The Jk(a-b-) phenotype, characterized by the absence of these antigens, is a rare blood group phenotype with a low population frequency, and its molecular basis is primarily associated with variants in the SLC14A1 gene. Herein, we identified an individual with the Jk(a-b-) phenotype carrying a variant, and evaluated whether this variant affects Jk antigen expression. Methods The Jk(a-b-) phenotype was identified by conventional serological typing. The coding sequence of the SLC14A1 gene was analyzed using polymerase chain reaction sequence-based typing (PCR-SBT), and haplotype analysis was performed using single-molecule sequencing. The functional impact of the variant was evaluated through in vitro transfection and expression assays, and Jk b antigen expression on transfected cells was assessed by flow cytometry. The potential functional impact of the variant was also evaluated using in silico prediction tools. Results Jk a , Jk b and Jk3 antigens were absent in the proband. PCR-SBT identified three heterozygous single-nucleotide variants (SNVs) and two homozygous SNVs across four exons of the SLC14A1 gene. Single-molecule sequencing revealed two haplotypes: one comprising c.342-1G>A, c.588A>G, and c.838G>A, and the other comprising c.230G>A, c.499A>G, c.588A>G, and c.838G>A. In silico analysis predicted c.230G>A to be a deleterious variant and indicated that it altered interactions with neighboring atoms. Functional assays showed that cells transfected with JK(c.230G>A+c.499A>G+c.588A>G+c.838G>A) did not express the Jk b antigen, while cells transfected with the JK*02 allele or JK(c.499A>G+c.588A>G+c.838G>A) exhibited high levels of Jk b antigen expression. Conclusions A JK null allele and its critical SNV were identified, and the functional effect of the variant was confirmed through transfection and expression studies.

Frontiers in ImmunologyVol. 17
Blood Center of Zhejiang Province (CN)
Good health and well-being
Openalex Percentile: Top 12%
Blood groups and transfusion
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