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

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

  • Sci Rep. 2017 Jun 15;7(1):3556. doi: 10.1038/s41598-017-03856-w.
Bailing Yan 1 Feng Chen 2 Lijun Xu 3 Yanshi Wang 4 Xuefu Wang 5 6
Affiliations

Affiliations

  • 1 Department of Emergency, The First Hospital of Jilin University, Changchun, 130021, China.
  • 2 Dermatology Department, China-Japan Union Hospital of Jilin University, Changchun, 130033, China.
  • 3 Department of Respiratory Medicine, The First Hospital of Jilin University, Changchun, 130021, China. lijunxu001@sina.com.
  • 4 Institute of Immunology, School of Life Sciences, University of Science and Technology of China, Hefei, Anhui, 230027, China.
  • 5 Institute of Immunology, School of Life Sciences, University of Science and Technology of China, Hefei, Anhui, 230027, China. wangxuefu@ustc.edu.cn.
  • 6 School of Pharmacology, Anhui Medical University, Hefei, Anhui, 230032, China. wangxuefu@ustc.edu.cn.
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.

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