芝加哥洛约拉大学Yee Ling Wu研究小组报道了肺驻留记忆B细胞维持呼吸道的过敏性IgE反应。相关论文于2025年3月25日发表在《免疫学》杂志上。

小组研究了支持呼吸道产生IgE的细胞机制。吸入过敏原可引起B细胞向肺部浸润和气道内的IgE。追踪报告小鼠中准备转换IgE类别的B细胞，发现肺中主要的IgE类别转换，并鉴定出IgG1⁺ MBCs是产生IgE的细胞的前体，这得到了B细胞受体（BCR）库测序的支持。B细胞与CD4⁺ T细胞定位于细支气管周围淋巴样聚集体。在共培养中，来自肺Th2细胞的白细胞介素-4诱导肺MBCs转换为IgE。异种共生表明，抗原再攻毒后，肺内居住的MBCs扩张，同时出现IgE分泌浆细胞（PCs），气道内IgE的产生不依赖于循环中的全身IgE。它们，肺内的IgG1⁺ MBCs是呼吸粘膜分泌IgE的PCs的细胞前体。

据介绍，虽然过敏原特异性免疫球蛋白E （IgE）是过敏性哮喘的关键介质，但表达IgE的B细胞不能形成记忆B细胞（MBCs）。

附：英文原文

Title: Lung-resident memory B cells maintain allergic IgE responses in the respiratory tract

Author: Alexander J. Nelson, Bruna K. Tatematsu, Jordan R. Beach, Dorothy K. Sojka, Yee Ling Wu

Issue&Volume: 2025-03-25

Abstract: Although allergen-specific immunoglobulin E (IgE) is a key mediator of allergic asthma, IgE-expressing B cells fail to form memory B cells (MBCs). Here, we studied the cellular mechanisms supporting IgE production in the respiratory tract. Allergen inhalation induced B cell infiltration into the lungs and IgE in the airway. Tracking B cells poised to class switch to IgE in reporter mice revealed predominant IgE class switching in the lung and identified IgG1+ MBCs as precursors of IgE-producing cells, which was supported by B cell receptor (BCR) repertoire sequencing. B cells localized with CD4+ T cells in peribronchiolar lymphoid aggregates. In coculture, interleukin-4 from lung Th2 cells induced lung MBCs to class switch to IgE. Lung-resident MBCs expanded after antigen rechallenge, concurrent with the emergence of IgE-secreting plasma cells (PCs), and the production of IgE in the airway was independent of systemic IgE in circulation, as indicated by parabiosis. Thus, lung-resident IgG1+ MBCs are cellular precursors for IgE-secreting PCs in the respiratory mucosa.

DOI: 10.1016/j.immuni.2025.03.001

Source: https://www.cell.com/immunity/abstract/S1074-7613(25)00095-0