Liu Qiao, Bin Dong-Hua, Wang Zhuo-Ya, Peng Ke-Ping, Tang Wang, Huang Jing-Weng, Xu Ling-Zhi, Wang Xiang-Yu, Yang Ping-Chang, Tian Gui-Xiang
Department of Ultrasoud, The Second Xiangya Hospital of Central South University, Changsha, China.
Department of Anus and Intesine, The First Hospital of Hunan University of Chinese Medicine, Changsha, China.
Immunology. 2025 Jan;174(1):128-138. doi: 10.1111/imm.13868. Epub 2024 Oct 9.
Dysfunctional immune regulation contributes to the pathogenesis of food allergy (FA). The mechanism behind regulatory B-cell dysfunction is unclear. CpG has immune regulatory functions. The purpose of this study is to use CpG to recover the immune suppressive functions of B cells in mice with FA. An FA mouse model was created using ovalbumin as the specific antigen. Flow cytometry was used to isolate B cells from the intestinal tissues. The immune regulatory functions of B cells were assessed using immunological approaches. The results showed that the FA response was linked to low IL-10 levels in gut lavage fluids of FA mice. FA mouse intestinal B cells produced lower amounts of IL-10 as compared with B cells isolated from naïve control mice. Impaired immune suppressive functions were observed in B cells isolated from the FA mouse intestine. The inducibility of the Il10 expression in naïve B cells of the intestine of FA mice was defective. The induction of Il10 expression in FA B cells could be restored by CpG through regulating the methylation status of the Cmip promoter. CpG promoted the therapeutic efficacy of allergen specific immunotherapy by restoring the induction of IL-10 B cells in the intestine. The expression of Il10 in B cells of the FA mouse intestine was impaired. Administration of CpG could restore the expression of Il10 in B cells in the intestine and promote immunotherapy for FA.
免疫调节功能障碍参与食物过敏（FA）的发病机制。调节性B细胞功能障碍背后的机制尚不清楚。CpG具有免疫调节功能。本研究的目的是使用CpG恢复FA小鼠中B细胞的免疫抑制功能。以卵清蛋白作为特异性抗原建立FA小鼠模型。采用流式细胞术从肠道组织中分离B细胞。使用免疫学方法评估B细胞的免疫调节功能。结果表明，FA反应与FA小鼠肠道灌洗液中低水平的IL-10有关。与从单纯对照小鼠分离的B细胞相比，FA小鼠肠道B细胞产生的IL-10量更低。在从FA小鼠肠道分离的B细胞中观察到免疫抑制功能受损。FA小鼠肠道幼稚B细胞中Il10表达的诱导能力存在缺陷。CpG可通过调节Cmip启动子的甲基化状态恢复FA B细胞中Il10的表达。CpG通过恢复肠道中IL-10+B细胞的诱导来促进变应原特异性免疫治疗的疗效。FA小鼠肠道B细胞中Il10的表达受损。给予CpG可恢复肠道B细胞中Il10的表达，并促进FA的免疫治疗。
