CD23 expression on switched memory B cells bridges T-B cell interaction in allergic rhinitis
CD23 expression on switched memory B cells bridges T-B cell interaction in allergic rhinitis
复制标题
切换记忆 B 细胞上的 CD23 表达在过敏性鼻炎中桥接 T-B 细胞相互作用
作者：
Yao Yin;Wang Nan;Chen Cai-Ling;Pan Li;Wang Zhi-Chao;Yunis Joseph;Chen Zhi-An;Zhang Yu;Hu Si-Tao;Xu Xiao-Yan;Zhu Rong-Fei;Yu Di;Liu Zheng
B细胞亚群和T-B细胞相互作用在变应性鼻炎(AR)发病机制和过敏原免疫治疗(AIT)机制中的作用尚不清楚。本研究旨在探讨急性呼吸窘迫综合征(ARB)患者循环中B细胞的特征、机制及其与AIT临床疗效的关系。方法采用IgD/CD27和CD24/CD38核心门控系统检测B细胞的频率和表型。研究AR患者B细胞、T细胞、抗原特异性IgE与疾病严重程度的相关性。开关记忆B细胞与2型滤泡辅助性T细胞(Tfh2)和卵泡调节性T细胞(Tfr)共培养。分析B细胞亚群与AIT临床益处的关系。结果AR患者循环记忆B细胞的频率和绝对数增加。AR患者CD19+CD2 0+CD2 7+IGD−交换记忆B细胞表面CD2 3表达显著增强，并与抗原特异性IgE水平、症状积分、TfH2/TfR细胞比值呈正相关。与健康对照组相比，AR患者的Tfh2细胞具有更强的IL-4诱导转换记忆B细胞CD23表达的能力，而IL-10表达缺陷的AR相关TFR细胞不能充分抑制这种能力。结论T-B细胞间的相互作用可能参与了AR患者AIT的发病机制，T-B细胞间的相互作用可能与AR患者AIT的发病有关。
BackgroundThe contribution of B‐cell subsets and T‐B cell interaction to the pathogenesis of allergic rhinitis (AR) and mechanisms of allergen immunotherapy (AIT) remain poorly understood. This study aimed to outline circulating B‐cell signature, the underlying mechanism, and its association with clinical response to AIT in patients with AR.MethodsIgD/CD27 and CD24/CD38 core gating systems were used to determine frequencies and phenotypes of B cells. Correlations between B cells, T cells, antigen‐specific IgE, and disease severity in AR patients were investigated. Switched memory B cells were co‐cultured with type 2 follicular helper T (Tfh2) cells and follicular regulatory T (Tfr) cells. Associations between B‐cell subsets and clinical benefits of AIT were analyzed.ResultsFrequencies and absolute numbers of circulating memory B cells were increased in AR patients. CD23 expression on CD19+CD20+CD27+IgD−switched memory B cells was significantly enhanced and positively correlated with antigen‐specific IgE levels, symptom scores, and Tfh2/Tfr cell ratio in AR patients. Compared with those from healthy controls, Tfh2 cells from AR patients had a greater capacity to induce CD23 expression on switched memory B cells via IL‐4, which was unable to be sufficiently suppressed by AR‐associated Tfr cells with defective IL‐10 expression. CD23 expression on switched memory B cells was downregulated after 12‐month AIT, which positively associated with disease remission in AR patients.ConclusionT‐B cell interaction, bridged by CD23 expression particularly on switched memory B cells, may be involved in the disease pathogenesis and mechanism of AIT in patients with AR.