该研究团队假设C型凝集素DC-SIGN可能直接与FcγRIIB上的聚糖相互作用，增强其结合唾液化IgG的能力。该研究组发现，Fc工程唾液化IgG1以增强其对FcγRIIB的亲和力，从而产生一种比IVIG更有效的分子，可以减少抗体或T细胞介导的自身免疫性疾病的炎症后遗症，为一类有效的抗炎治疗提供基础。
据介绍，高剂量静脉注射免疫球蛋白（IVIG）被用于治疗多种自身免疫性疾病。小鼠模型研究发现，IVIG的抗炎活性依赖于免疫球蛋白G （IgG）、I型IgG抑制Fc受体FcγRIIB和II型Fc受体树突状细胞特异性细胞间粘附分子-3-捕获非整合素（DC-SIGN）的CH2结构域上N-链聚糖的唾液酰化。
附：英文原文
Title: The anti-inflammatory activity of IgG is enhanced by co-engagement of type I and II Fc receptors
Author: Andrew T. Jones, Alessandra E. Marino, Tetyana Martynyuk, Stylianos Bournazos, Jeffrey V. Ravetch
Issue&Volume: 2025-11-06
Abstract: Intravenous immunoglobulin (IVIG) administered at high doses is used to treat a wide array of autoimmune diseases. Studies in murine models have identified that the anti-inflammatory activity of IVIG is dependent on sialylation of the N-linked glycan on the CH2 domain of immunoglobulin G (IgG), the type I IgG inhibitory Fc receptor FcγRIIB, and the type II Fc receptor dendritic cell-specific intercellular adhesion molecule-3-grabbing non-integrin (DC-SIGN). We hypothesized that DC-SIGN, a C-type lectin, may directly interact with glycans on FcγRIIB, augmenting its ability to bind sialylated IgG. We found that Fc-engineering sialylated IgG1 to enhance its affinity for FcγRIIB resulted in a molecule that was more potent than IVIG in reducing the inflammatory sequelae of antibody or T cell–mediated autoimmune diseases, providing the basis for a class of potent anti-inflammatory therapeutics.
DOI: adv2927
Source: https://www.science.org/doi/10.1126/science.adv2927