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白细胞介素-28B 通过上调自然杀伤细胞衍生的 IFN-γ 抑制气道炎症。

Interleukin-28B dampens airway inflammation through up-regulation of natural killer cell-derived IFN-γ.

机构信息

Department of Emergency, The First Hospital of Jilin University, Changchun, 130021, China.

Dermatology Department, China-Japan Union Hospital of Jilin University, Changchun, 130033, China.

出版信息

Sci Rep. 2017 Jun 15;7(1):3556. doi: 10.1038/s41598-017-03856-w.

Abstract

Interleukin-28A (IL-28A) modulates CD11c+ dendritic cell (DC) function and promotes type 1T helper (Th1) differentiation, thus suppressing allergic airway diseases. However, the function of the IL-28A isoform IL-28B in these diseases remains largely unknown. In this study, we revealed a novel role of IL-28B in inducing type 1 immunity and protecting against ovalbumin (OVA)-induced allergic asthma in mice. IL-28B overexpression in wild-type mice promoted natural killer (NK) cell polarization in the lung, leading to the increased number of interferon (IFN)-γ-producing NK1 cells as well as Th1 differentiation. Importantly, IL-28B overexpression had no protective effect on OVA-induced asthma in IFN-γ-knockout (IFN-γ-/-) mice. These results demonstrate that IL-28B ameliorates experimental allergic asthma via enhancing NK cell polarization, which might be useful for prevention and treatment of allergic asthma.

摘要

白细胞介素-28A(IL-28A)调节 CD11c+树突状细胞(DC)功能,促进 1 型 T 辅助(Th1)分化,从而抑制过敏性气道疾病。然而,IL-28A 同种型 IL-28B 在这些疾病中的功能在很大程度上仍然未知。在这项研究中,我们揭示了 IL-28B 在诱导 1 型免疫和保护小鼠卵清蛋白(OVA)诱导的过敏性哮喘中的新作用。在野生型小鼠中过表达 IL-28B 可促进肺中自然杀伤(NK)细胞的极化,导致 IFN-γ 产生的 NK1 细胞数量增加以及 Th1 分化。重要的是,IL-28B 过表达对 IFN-γ 敲除(IFN-γ-/-)小鼠的 OVA 诱导的哮喘没有保护作用。这些结果表明,IL-28B 通过增强 NK 细胞极化来改善实验性过敏性哮喘,这可能有助于预防和治疗过敏性哮喘。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/73c4/5472588/727d3a7e085a/41598_2017_3856_Fig1_HTML.jpg

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