Interleukin-28B dampens airway inflammation through up-regulation of natural killer cell-derived IFN-γ
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 nov...
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| Autores principales: | , , , , |
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| Formato: | article |
| Lenguaje: | EN |
| Publicado: |
Nature Portfolio
2017
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| Materias: | |
| Acceso en línea: | https://doaj.org/article/7926dae70b104e618ffe6f9fc41769ca |
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| Sumario: | 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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