Alavi A, Axford J
Division of Immunology, St George's Hospital Medical School, London, UK.
Glycoconj J. 1995 Jun;12(3):206-10. doi: 10.1007/BF00731321.
Evidence indicating an important link between glycosylation changes and autoimmune rheumatic disease is presented. Attention is especially focused on the interrelationship between reduced galactosylation of the oligosaccharides of IgG, auto-sensitization which is thought to be of central importance in the pathogenesis of rheumatoid arthritis (RA), and the enzyme beta 1,4-galactosyltransferase (GTase) that catalyses the addition of galactose to the oligosaccharide chains on this molecule. Data are presented to indicate that GTase undergoes a variety of normal and disease associated changes. These variations are believed to contribute to the pathological processes in rheumatoid disease, and a hypothesis is suggested, whereby disease is associated with the dysregulation of an integrated glycosylation network, comprising IgG galactosylation, lymphocytic GTase and anti-GTase antibodies, that is a component of the normal immune system.
本文展示了表明糖基化变化与自身免疫性风湿性疾病之间存在重要联系的证据。特别关注的是IgG寡糖半乳糖基化减少、自身致敏（这被认为在类风湿性关节炎（RA）发病机制中至关重要）以及催化半乳糖添加到该分子寡糖链上的β1,4-半乳糖基转移酶（GTase）之间的相互关系。文中呈现的数据表明GTase会发生各种正常及与疾病相关的变化。这些变化被认为促成了类风湿性疾病中的病理过程，并提出了一个假说，即疾病与一个整合糖基化网络的失调相关，该网络包括IgG糖基化、淋巴细胞GTase和抗GTase抗体，而这是正常免疫系统的一个组成部分。
