Porcine Fc gamma receptor IIb (FcγRIIb) has been cloned and characterized for many years. However, the role of FcγRIIb in innate antiviral response to porcine reproductive and respiratory syndrome virus (PRRSV) infection has not yet been well investigated. In current study, our results showed that specific activation of FcγRIIb in porcine alveolar macrophages (PAMs) significantly enhanced the production of interferon-alpha (IFN-α) and interferon-gamma (IFN-γ), and significantly repressed the production of transforming growth factor beta 1 (TGF-β1). In addition, our results showed that specific activation of FcγRIIb in PAMs cells in PRRSV infection not only significantly increased the production of IFN-α and IFN-γ, but also significantly decreased the production of TGF-β1, and significantly inhibited PRRSV replication level. In summary, our studies indicated that FcγRIIb signaling up-regulated the production of IFN-α and IFN-γ in PAMs cells in vitro, in response to PRRSV infection.

中文翻译：

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在 PRRSV 感染期间，Fc γ 受体 IIb 的激活上调了猪肺泡巨噬细胞中干扰素-α 和干扰素-γ 的产生。

猪 Fc γ 受体 IIb (FcγRIIb) 已被克隆和表征多年。然而，FcγRIIb 在对猪繁殖与呼吸综合征病毒 (PRRSV) 感染的先天抗病毒反应中的作用尚未得到很好的研究。在目前的研究中，我们的结果表明，猪肺泡巨噬细胞 (PAMs) 中 FcγRIIb 的特异性激活显着增强了干扰素-α (IFN-α) 和干扰素-γ (IFN-γ) 的产生，并显着抑制了转化生长的产生。因子β1（TGF-β1）。此外，我们的结果表明，PRRSV感染PAMs细胞中FcγRIIb的特异性激活不仅显着增加了IFN-α和IFN-γ的产生，而且显着降低了TGF-β1的产生，并显着抑制了PRRSV复制水平。总之，