肺驻留记忆B细胞维持呼吸道过敏IgE应答
2025/07/15
摘要：
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（MBC）。本研究探讨了支持呼吸道产生IgE的细胞机制。吸入变应原会诱导B细胞浸润到肺部，并在气道中产生IgE。通过在报告小鼠中追踪准备向IgE类别转换的B细胞，揭示了肺中发生了重要的IgE类别转换，并鉴定出IgG1+ MBC为产生IgE的前体细胞，这一发现得到了B细胞受体（BCR）库测序的支持。B细胞与CD4+ T细胞共定位于支气管周围淋巴聚集体中。在共培养中，来自肺Th 2细胞的IL-4诱导肺MBCs向IgE类别转换。抗原再次刺激后，肺部驻留MBCs扩增，同时出现分泌IgE的浆细胞（PC）；通过联体共生实验表明，气道中IgE的产生独立于循环中的全身IgE。因此，肺驻留IgG 1 + MBC是呼吸道粘膜中分泌IgE的PC的细胞前体。
Lung-resident memory B cells maintain allergic IgE responses in the respiratory tract
Nelson, A. J., Tatematsu, B. K., Beach, J. R., Sojka, D. K, et al.
Immunity, 58(4), 875–888.e8. https://doi.org/10.1016/j.immuni.2025.03.001.
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 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.
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（MBC）。本研究探讨了支持呼吸道产生IgE的细胞机制。吸入变应原会诱导B细胞浸润到肺部，并在气道中产生IgE。通过在报告小鼠中追踪准备向IgE类别转换的B细胞，揭示了肺中发生了重要的IgE类别转换，并鉴定出IgG1+ MBC为产生IgE的前体细胞，这一发现得到了B细胞受体（BCR）库测序的支持。B细胞与CD4+ T细胞共定位于支气管周围淋巴聚集体中。在共培养中，来自肺Th 2细胞的IL-4诱导肺MBCs向IgE类别转换。抗原再次刺激后，肺部驻留MBCs扩增，同时出现分泌IgE的浆细胞（PC）；通过联体共生实验表明，气道中IgE的产生独立于循环中的全身IgE。因此，肺驻留IgG 1 + MBC是呼吸道粘膜中分泌IgE的PC的细胞前体。
（四川大学华西医院呼吸与危重症医学科 林红霞 王霁 王刚 译）
（Immunity, 58(4), 875–888.e8. https://doi.org/10.1016/j.immuni.2025.03.001.）
Lung-resident memory B cells maintain allergic IgE responses in the respiratory tract
Nelson, A. J., Tatematsu, B. K., Beach, J. R., Sojka, D. K, et al.
Immunity, 58(4), 875–888.e8. https://doi.org/10.1016/j.immuni.2025.03.001.
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 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.
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