Integrated bioinformatic analysis revealed biological processes and immune cells implicated in autoimmune hepatitis

Integrated bioinformatic analysis revealed biological processes and immune cells implicated in autoimmune hepatitis
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综合生物信息分析揭示了与自身免疫性肝炎有关的生物过程和免疫细胞

DOI:
10.1002/jcp.30246
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发表时间:
2021-02-17
影响因子:
5.6
通讯作者:
Li,Ning
Li,Ning
中科院分区:
生物学2区
文献类型:
--
作者:
Yu,Kangkang;Yang,Jingshu;Li,Ning

文献摘要

相似文献

自身免疫性肝炎(AIH)是一种免疫介导的炎症性肝病,其发病机制尚不完全清楚。本研究旨在通过综合生物信息学分析揭示与AIH有关的关键生物学过程和免疫细胞。通过基因芯片数据分析,研究了野生型BALB/c小鼠、Tgfb1缺陷小鼠以及Tgfb1和Ifng2两种缺陷小鼠肝脏的整体基因表达。对差异表达基因进行鉴定,并进行功能浓缩分析。同时缺失Tgfb1和Ifng的AIH小鼠免疫反应显著增强,代谢过程受损,T细胞活化和细胞因子产生增加,有机酸和脂代谢过程减弱。用CiberSort法检测免疫细胞的渗入情况。观察到AIH小鼠T细胞、巨噬细胞和自然杀伤细胞的浸润增加,中性粒细胞、嗜酸性粒细胞、浆细胞和B细胞的渗透减少。总之,我们确定了导致AIH的潜在生物学过程和免疫细胞;需要进一步的研究来证实这些发现,从而为AIH的治疗提供一个潜在的新的治疗靶点。
Autoimmune hepatitis (AIH) is an immune‐mediated inflammatory liver disease for which the pathogenesis remains incompletely understood. The current study aimed to reveal key biological processes and immune cells implicated in AIH by integrated bioinformatic analysis. The global gene expression in livers from wild‐type BALB/c mice, mice withTgfb1deficiency, and mice with bothTgfb1andIfngdeficiency was assessed by microarray data analysis. Differentially expressed genes were identified and subjected to functional enrichment analysis. AIH mice withTgfb1deletion showed significantly enhanced immune responses but impaired metabolic processes, whereas increased T cell activation and cytokine production, but weakened organic acid and lipid metabolic processes were observed in mice with deletion of bothTgfb1andIfng. In addition, infiltration of immune cells was evaluated by CIBERSORT. Increased infiltration of T cells, macrophages, and natural killer cells, and decreased infiltration of neutrophils, eosinophils, plasma cells, and B cells were observed in AIH mice. In conclusion, we identified potential biological processes and immune cells that contributed to AIH; further investigations are needed to confirm these findings and thus provide a potential novel therapeutic target for AIH treatment.