结肠炎
炎症性肠病
炎症
免疫印迹
车站3
免疫系统
免疫学
细胞因子
医学
生物
信号转导
内科学
疾病
细胞生物学
生物化学
基因
作者
Shouzhi Zhou,Zhao Yang,Jiaxin Liu,Maojuan Ran
标识
DOI:10.1016/j.imlet.2023.02.005
摘要
TIPE-2 has been identified as a negative regulator of both innate and adaptive immunity and is involved in several inflammatory diseases. However, the immune inhibition mechanism of TIPE-2 involved in inflammatory bowel disease has not been well studied. Therefore, the aim of this study was to investigate whether TIPE-2 improved experimental colitis by reducing high levels of inflammation in the intestine. Lentivirus encoding TIPE-2 was administered to mice by intrarectal injection after colitis induction. Histological analysis was used to analyze sections of the intestine. Protein expression induced by STAT3 and NF-κB signaling was analyzed by western blot. We found that TIPE-2 reduced the colitis activity index score and the histological score of the intestine. TIPE-2 also decreased inflammatory cytokine levels in the intestine. Additionally, TIPE-2 inhibited STAT3 and NF-kB activation. These results suggested that TIPE-2 might attenuate inflammation of colitis via inhibiting of STAT3 and NF-kB activation.
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