Role of IL-10-producing regulatory B cells in modulating T-helper cell immune responses during silica-induced lung inflammation and fibrosis.
Role of IL-10-producing regulatory B cells in modulating T-helper cell immune responses during silica-induced lung inflammation and fibrosis.
复制标题
二氧化硅诱导的肺部炎症和纤维化过程中，产生 IL-10 的调节性 B 细胞在调节 T 辅助细胞免疫反应中的作用。
DOI：
10.1038/srep28911
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发表时间：
2016-06-29
影响因子：
4.6
通讯作者：
Chen J
中科院分区：
文献类型：
--
作者：
Liu F;Dai W;Li C;Lu X;Chen Y;Weng D;Chen J
矽肺以肺部慢性炎症和纤维化为特征，严重危害人体健康。先前的研究表明，不受控制的辅助性 T 细胞 (Th) 细胞免疫反应与矽肺的发病机制有关。据报道，淋巴细胞也发挥着重要作用。现有关于淋巴细胞调节Th免疫反应的研究仅限于T细胞，例如调节性T（Treg）细胞，它可以负向调节炎症并促进矽肺病的进程。然而，矽肺中的其他调节子集尚未得到详细研究，免疫稳态调节机制需要进一步探索。另一种调节性淋巴细胞，即调节性 B 细胞，最近引起了越来越多的关注。在这项研究中，我们全面展示了产生IL-10的调节性B细胞（B10）在小鼠矽肺模型中的作用。 B10 可通过二氧化硅滴注诱导。 B10 不足会促进 Th1 免疫反应，从而加剧炎症并减轻肺纤维化。 B10 不足会明显抑制 Treg 并降低 IL-10 水平。我们的研究表明，B10 可以通过抑制 Th1 反应和调节 Th 平衡来控制肺部炎症并加剧肺纤维化。 B10 的调节功能可能与 Treg 诱导和 IL-10 分泌有关。
Silicosis is characterized by chronic lung inflammation and fibrosis, which are seriously harmful to human health. Previous research demonstrated that uncontrolled T-helper (Th) cell immune responses were involved in the pathogenesis of silicosis. Lymphocytes also are reported to have important roles. Existing studies on lymphocyte regulation of Th immune responses were limited to T cells, such as the regulatory T (Treg) cell, which could negatively regulate inflammation and promote the process of silicosis. However, other regulatory subsets in silicosis have not been investigated in detail, and the mechanism of immune homeostasis modulation needs further exploration. Another regulatory lymphocyte, the regulatory B cell, has recently drawn increasing attention. In this study, we comprehensively showed the role of IL-10-producing regulatory B cell (B10) in a silicosis model of mice. B10 was inducible by silica instillation. Insufficient B10 amplified inflammation and attenuated lung fibrosis by promoting the Th1 immune response. Insufficient B10 clearly inhibited Treg and decreased the level of IL-10. Our study indicated that B10 could control lung inflammation and exacerbate lung fibrosis by inhibiting Th1 response and modulating the Th balance. The regulatory function of B10 could be associated with Treg induction and IL-10 secretion.