Regulatory B cells induced by ultraviolet B through toll-like receptor 4 signalling contribute to the suppression of contact hypersensitivity responses in mice
Regulatory B cells induced by ultraviolet B through toll-like receptor 4 signalling contribute to the suppression of contact hypersensitivity responses in mice
复制标题
紫外线 B 通过 Toll 样受体 4 信号传导诱导调节性 B 细胞有助于抑制小鼠接触超敏反应
DOI：
10.1111/cod.12913
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发表时间：
2018
影响因子：
5.5
通讯作者：
Dou X
中科院分区：
文献类型：
--
作者：
Liu X;Huang H;Gao H;Wu X;Zhang W;Yu B;Dou X
背景紫外线（UV）B照射可通过抑制小鼠的免疫反应来抑制接触性超敏反应（CHS）。然而，负责UVB诱导的系统性抑制的细胞机制仍不清楚。据报道，调节性B细胞在CHS期间起抑制作用。目的探讨UVB照射对调节性B细胞的诱导作用及其机制。方法采用恶唑酮诱导CHS小鼠模型，通过组织病理学、流式细胞术和真实的定量聚合酶链反应（RT-PCR）等方法，观察UVB照射对调节性B细胞的诱导作用，并观察UVB照射对CHS小鼠的影响。UVB诱导的调节性B细胞通过抑制T细胞增殖而导致全身免疫抑制。此外，我们确定，Toll样受体（TLR）4，其中的表达是在B细胞UVB照射后上调，在诱导调节B celles.ConclusionOur的数据确定调节B细胞作为调节剂的UVB诱导的免疫抑制CHS，并建议的重要性的UVB-TLR 4轴在调节B细胞的产生。
BackgroundUltraviolet (UV) B irradiation is known to suppress contact hypersensitivity (CHS) responses in mouse models by suppressing immune responses. However, the cellular mechanisms responsible for UVB‐induced systemic suppression remain unclear. Regulatory B cells have been reported to play an inhibitory role during CHS. It is presently unknown whether regulatory B cells contribute to the effect of UVB phototherapy.ObjectiveTo investigate the inductive effect of UVB on regulatory B cells and the underlying mechanisms by using a CHS mouse model.MethodsCHS was induced with oxazolone, and evaluated by histopathology, flow cytometry, and quantitative real‐time polymerase chain reaction.ResultWe found that UVB irradiation induced regulatory B cell expansion and ameliorated CHS. UVB‐induced regulatory B cells contribute to systemic immunosuppression by inhibiting the proliferation of T cells. Moreover, we determined that toll‐like receptor (TLR) 4, the expression of which was upregulated in B cells after UVB exposure, played an essential role in the induction of regulatory B cells.ConclusionOur data identified regulatory B cells as regulators of UVB‐induced immunosuppression in CHS, and suggest the importance of the UVB–TLR4 axis in the generation of regulatory B cells.