Twin studies on the effect of genetic factors on serum agalactosyl immunoglobulin G levels
- Authors:
- Kanako Azuma
- Shinichiro Shinzaki
- Hitomi Asazawa
- Eri Kuroki
- Sayuri Kawamoto
- Yoshihiro Kamada
- Kazuo Hayakawa
- Eiji Miyoshi
View Affiliations
Affiliations: Department of Molecular Biochemistry and Clinical Investigation, Osaka University Graduate School of Medicine, Suita, Osaka 565‑0871, Japan, Department of Health Promotion Science, Osaka University Graduate School of Medicine, Suita, Osaka 565‑0871, Japan
- Published online on: January 3, 2014 https://doi.org/10.3892/br.2014.216
-
Pages:
213-216
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Abstract
The level of immunoglobulin G (IgG) lacking the terminal galactose, referred to as agalactosyl IgG, was found to be increased in chronic inflammatory diseases, such as rheumatoid arthritis and inflammatory bowel disease (IBD), particularly in Crohn's disease, which is suggested to have a genetic component. This oligosaccharide modification of IgG is mainly regulated by the expression of glyco‑genes; however, the association between genetic factors and changes in the IgG glycosylation has not been fully elucidated. The aim of the present study was to assess the role of genetics in this process by comparing the serum agalactosyl IgG levels between members of monozygotic and dizygotic twin pairs who underwent medical check‑ups at the same time. The serum agalactosyl IgG level was assayed using high‑performance liquid chromatography. Hematological and biochemical markers, including γ‑glutamyltranspeptidase (γGTP), alanine aminotransferase (ALT) and white blood cell (WBC) count, were also measured. Although the serum γGTP levels (and, to a lesser extent, ALT and WBC levels) exhibited a correlation within monozygotic twin pairs, agalactosyl IgG levels were not found to be correlated between members of either type of twin pairs. Thus, the role of genetic factors in determining serum agalactosyl IgG levels may be less significant compared to the effect of environmental factors or the onset of inflammatory disease.
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