Immunoglobulin glycosylation is a pivotal mechanism that drives the diversification of antibody functions. The composition of the IgG glycome is influenced by environmental factors, genetic traits and inflammatory contexts. Differential IgG glycosylation has been shown to intricately modulate IgG effector functions and has a role in the initiation and progression of various diseases. Analysis of IgG glycosylation is therefore a promising tool for predicting disease severity. Several autoimmune and alloimmune disorders, including critical and potentially life-threatening conditions such as systemic lupus erythematosus, anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis and antibody-mediated kidney graft rejection, are driven by immunoglobulin. In certain IgG-driven kidney diseases, including primary membranous nephropathy, IgA nephropathy and lupus nephritis, particular glycome characteristics can enhance in situ complement activation and the recruitment of innate immune cells, resulting in more severe kidney damage. Hypofucosylation, hypogalactosylation and hyposialylation are the most common IgG glycosylation traits identified in these diseases. Modulating IgG glycosylation could therefore be a promising therapeutic strategy for regulating the immune mechanisms that underlie IgG-driven kidney diseases and potentially reduce the burden of immunosuppressive drugs in affected patients.

免疫球蛋白糖基化是推动抗体功能多样化的关键机制。 IgG 糖组的组成受到环境因素、遗传特征和炎症环境的影响。差异 IgG 糖基化已被证明可以复杂地调节 IgG 效应子功能，并在各种疾病的发生和进展中发挥作用。因此，IgG 糖基化分析是预测疾病严重程度的有前途的工具。多种自身免疫性疾病和同种免疫性疾病，包括危重和可能危及生命的疾病，如系统性红斑狼疮、抗中性粒细胞胞浆抗体（ANCA）相关血管炎和抗体介导的肾移植排斥反应，都是由免疫球蛋白驱动的。在某些 IgG 驱动的肾脏疾病中，包括原发性膜性肾病、IgA 肾病和狼疮性肾炎，特定的糖组特征可以增强原位补体激活和先天免疫细胞的募集，从而导致更严重的肾脏损伤。低岩藻糖基化、低半乳糖基化和低唾液酸化是这些疾病中最常见的 IgG 糖基化特征。因此，调节 IgG 糖基化可能是一种有前途的治疗策略，用于调节 IgG 驱动的肾脏疾病的免疫机制，并有可能减轻受影响患者的免疫抑制药物负担。