Institute of Medical Device Control, National Institutes for Food and Drug Control, 102629, Beijing, China.
School of Medical Lab Science and Life Science, Wenzhou Medical University, 325035, Wenzhou, China.
Sci Rep. 2018 Oct 18;8(1):15433. doi: 10.1038/s41598-018-33032-7.
The Gal antigen is synthesized by glycoprotein galactosyltransferase alpha 1, 3 (GGTA1) or (and) isoglobotrihexosylceramide 3 synthase (iGb3S). However, whether iGb3S deletion changes Gal epitope expression and immunological properties in animals is still not clear. The objective of this study was to develop iGb3S deficient mice, and characterize their Gal epitope expression and Gal epitope-related immunological properties. iGb3S gene knockout mice were generated on the C57BL/6 background using the bacterial artificial chromosome homology region recombination technique. Gal epitope expression in the iGb3S deficient mice was determined by using a monoclonal anti-Gal antibody. Immunological properties were analyzed by enzyme linked immune sorbent assay. It was found that Gal epitope expression was decreased from 5.19% to 21.74% in the main organs of iGb3S deficient mice, compared with that of C57BL/6 wild type mice, suggesting that the iGb3S gene participated to Gal epitope expression. However, iGb3S deletion alone did not cause significant changes in the immunological properties of iGb3S deficient mice with or without exogenous Gal antigen (Rabbit Red Blood Cell) stimulation. The data from this study suggest that the iGb3S gene likely contributes to Gal epitope expression, but may have a very weak effect on immunological properties of the iGb3S deficient mice.
Gal 抗原由糖蛋白半乳糖基转移酶 alpha1,3（GGTA1）或（和）岩藻糖基-β-1,3-半乳糖基转移酶（iGb3S）合成。然而，iGb3S 缺失是否会改变动物中 Gal 表位的表达和免疫特性仍不清楚。本研究旨在构建 iGb3S 缺失小鼠，并对其 Gal 表位表达和 Gal 表位相关免疫特性进行鉴定。利用细菌人工染色体同源重组技术，在 C57BL/6 背景下构建 iGb3S 基因敲除小鼠。利用单克隆抗-Gal 抗体检测 iGb3S 缺失小鼠主要器官中 Gal 表位的表达。采用酶联免疫吸附试验分析免疫特性。结果发现，与 C57BL/6 野生型小鼠相比，iGb3S 缺失小鼠主要器官中 Gal 表位的表达从 5.19%降低至 21.74%，表明 iGb3S 基因参与 Gal 表位的表达。然而，iGb3S 缺失单独作用并未导致在有或无外源性 Gal 抗原（兔红细胞）刺激时 iGb3S 缺失小鼠免疫特性发生显著变化。本研究数据表明，iGb3S 基因可能有助于 Gal 表位的表达，但对 iGb3S 缺失小鼠的免疫特性可能影响非常微弱。
