白细胞介素-34 驱动自身免疫性肝炎中巨噬细胞向 M2 表型极化。
Interleukin-34 drives macrophage polarization to the M2 phenotype in autoimmune hepatitis.
机构信息
Department of Gastroenterology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, China.
Department of Gastroenterology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, China.
出版信息
Pathol Res Pract. 2019 Aug;215(8):152493. doi: 10.1016/j.prp.2019.152493. Epub 2019 Jun 10.
BACKGROUND
Autoimmune hepatitis is a chronic inflammatory disease, the abnormal immunological function is the main pathogenesis. Interleukin-34 is a newly identified cytokine that shares the same receptor as colony stimulating factor-1.
METHODS
We used interleukin-34 knockout and wild-type mice in a Con A-induced hepatitis model and cocultured RAW264.7 macrophage cells with interleukin-34. We then detected associated inflammatory cytokine and chemokine levels to elucidate the role of interleukin-34.
RESULTS
In this study, we found that the loss of interleukin-34 resulted in higher sensitivity to Con A-induced hepatitis. RAW264.7 macrophage cells were able to differentiate to the M2 phenotype upon interleukin-34 stimulation.
CONCLUSIONS
We conclude that interleukin-34 may protect the liver from Con A-mediated hepatitis by driving M2 macrophage polarization and suppressing inflammation.
背景
自身免疫性肝炎是一种慢性炎症性疾病，异常的免疫功能是主要的发病机制。白细胞介素-34 是一种新发现的细胞因子，与集落刺激因子-1 具有相同的受体。
方法
我们使用白细胞介素-34 敲除和野生型小鼠的 Con A 诱导的肝炎模型，并用白细胞介素-34 共培养 RAW264.7 巨噬细胞。然后检测相关炎症细胞因子和趋化因子水平，以阐明白细胞介素-34 的作用。
结果
在这项研究中，我们发现白细胞介素-34 的缺失导致对 Con A 诱导的肝炎更敏感。白细胞介素-34 刺激可使 RAW264.7 巨噬细胞向 M2 表型分化。
结论
我们的结论是，白细胞介素-34 可能通过驱动 M2 巨噬细胞极化和抑制炎症来保护肝脏免受 Con A 介导的肝炎。
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