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J Med Virol. 2014 Jul;86(7):1105-12. doi: 10.1002/jmv.23934. Epub 2014 Mar 24.

BTNL2 associated with the immune response to hepatitis B vaccination in a Chinese Han population.

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  • 1National Laboratory of Medical Molecular Biology, Institute of Basic Medical Science, Chinese Academy of Medical Sciences, School of Basic Medicine, Peking Union Medical College, Beijing, China.

Abstract

No response to hepatitis B vaccination is a complex phenomenon, which is induced by the combinations of environmental and genetic factors. The aim of the study was to investigate the association between the polymorphisms of the butyrophilin-like 2 (BTNL2) gene and the immune response to hepatitis B vaccination in a Chinese Han population. A total of 7 single nucleotide polymorphisms in the BTNL2 gene were analyzed in 566 non-responders and 1,040 high-responders to hepatitis B vaccination. The alleles T, T, C, A, G of rs3763316, rs3763311, rs9268494, rs3806156, and rs2076530 were associated with no response to hepatitis B vaccination (P = 0.015, odds ratio (OR) = 1.20; P = 0.029, OR = 1.18; P = 2.00E-07, OR = 1.58; P = 0.002, OR = 1.27; P = 2.90E-06, OR = 1.41, respectively). Whereas, the alleles T, C of rs9268501 and rs3763313 played significantly protective roles in the immune response to hepatitis B vaccination (P = 0.007, OR = 0.81; P = 0.004, OR = 0.74). Besides, the risks of no response to hepatitis B vaccination were increased significantly among individuals harbored the haplotypes of G-T-A-T-C-A-G (P = 0.038, OR = 1.48), G-T-A-T-C (P < 0.0001, OR = 2.34), A-A (P < 0.0001, OR = 4.08), and C-G (P < 0.0001, OR = 4.75). However, the haplotype of G-C-A-T-C (P = 1.00E-04, OR = 0.54) exhibited a protective role in the immune response to hepatitis B vaccination in the study. These findings suggest that polymorphisms in the BTNL2 gene might play a vital role in determining the outcome of the immune response to hepatitis B vaccination.

© 2014 Wiley Periodicals, Inc.

KEYWORDS:

butyrophilin-like 2; haplotype; hepatitis B vaccination; linkage disequilibrium; polymorphism

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