Drug-induced liver injury (DILI), which refers to liver damage caused by a drug or its metabolites, has emerged as an important cause of acute liver failure (ALF) in recent years. Chemically-induced ALF in animal models mimics the pathology of DILI in humans; thus, these models are used to study the mechanism of potentially effective treatment strategies. Mesenchymal stromal cells (MSCs) possess immunomodulatory properties, and they alleviate acute liver injury and decrease the mortality of animals with chemically-induced ALF. Here, we summarize some of the existing research on the interaction between MSCs and immune cells, and discuss the possible mechanisms underlying the immuno-modulatory activity of MSCs in chemically-induced ALF. We conclude that MSCs can impact the phenotype and function of macrophages, as well as the differentiation and maturation of dendritic cells, and inhibit the proliferation and activation of T lymphocytes or B lymphocytes. MSCs also have immuno-modulatory effects on the production of cytokines, such as prostaglandin E2 and tumor necrosis factor-alpha-stimulated gene 6, in animal models. Thus, MSCs have significant benefits in the treatment of chemically-induced ALF by interacting with immune cells and they may be applied to DILI in humans in the near future.

中文翻译：

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化学诱导的急性肝衰竭中的间充质基质细胞依赖性免疫调节。

近年来，药物引起的肝损伤（DILI）是由药物或其代谢产物引起的肝损害，已成为急性肝衰竭（ALF）的重要原因。在动物模型中化学诱导的ALF模仿了人类DILI的病理。因此，这些模型用于研究潜在有效治疗策略的机制。间充质基质细胞（MSC）具有免疫调节特性，可减轻急性肝损伤并降低化学诱导ALF引起动物的死亡率。在这里，我们总结了一些有关MSC与免疫细胞之间相互作用的现有研究，并讨论了在化学诱导的ALF中MSC免疫调节活性的潜在机制。我们得出的结论是，MSC可以影响巨噬细胞的表型和功能，以及树突状细胞的分化和成熟，并抑制T淋巴细胞或B淋巴细胞的增殖和活化。MSC在动物模型中还对细胞因子（例如前列腺素E2和肿瘤坏死因子-α刺激的基因6）的产生具有免疫调节作用。因此，MSC通过与免疫细胞相互作用而在化学诱导的ALF的治疗中具有显着的益处，并且它们可以在不久的将来应用于人的DILI。