新型生物标志物可能会导致肝纤维化的早期检测

StephenW

Novel biomarker could potentially lead to early detection of liver fibrosis
Main Category: Liver Disease / Hepatitis
Article Date: 19 Aug 2013 - 0:00 PDT



Chronic liver disease is a leading cause of death in the United States, in part because it often causes the formation of harmful scar tissue - a process known as fibrosis. A study published by Cell Press in the journal Immunity reveals the central role the immune molecule interleukin 33 (IL-33) plays in the formation of liver fibrosis. The findings suggest that drugs targeting this molecule could serve as a new treatment strategy to protect against liver fibrosis.

"Currently, the therapeutic options for liver fibrosis are limited and not curative," says senior study author Stefan Wirtz of Friedrich-Alexander University Erlangen-Nuremberg. "We identified novel immunological factors that contribute to the development of liver fibrosis, opening up new avenues for the treatment of this serious condition."

Liver fibrosis refers to the accumulation of harmful deposits of extracellular matrix (ECM) proteins, and it can eventually lead to organ failure. Past studies have suggested that this kind of damage is associated with abnormal immune responses in the liver, but very little was known about the molecules and cells that contribute to fibrosis.

In the new study, Wirtz and his team found that the amount of IL-33 in the blood was higher than normal in patients with liver disease. Following up on this observation, they discovered that injection of IL-33 into mice caused ECM proteins to build up in the liver, whereas mice that were genetically modified to lack IL-33 were largely protected from fibrosis. The researchers went on to identify the immune networks underlying IL-33's harmful effects and discovered that this molecule activates immune cells called type 2 innate lymphoid cells (ILC2), which had never before been linked to liver disease.

"Our findings reveal IL-33 as a novel biomarker that could potentially lead to early detection of fibrosis in patients, which may be extremely valuable for preventing further damage to the liver," Wirtz says. "Moreover, the study shows that drugs targeting IL-33 or ILC2 responses could be a promising strategy to protect against fibrosis and chronic liver disease."


Immunity, Mchedlidze et al.: "Interleukin-33-Dependent Innate Lymphoid Cells Mediate Hepatic Fibrosis." 10.1016/j.immuni.2013.07.018

Cell Press

StephenW

新型生物标志物可能会导致肝纤维化的早期检测
主要分类：肝病/肝炎
文章日期：2013年8月19日 -  0:00 PDT


慢性肝病是一家领先的死因在美国，部分原因是因为它往往会导致有害的疤痕组织的形成 - 这个过程被称为纤维化。由细胞出版社出版的“免疫”杂志上的一项研究，揭示了免疫分子白细胞介素33（IL-33）在肝纤维化形成中起着核心作用。研究结果表明，这种分子靶向药物，可以作为一种新的治疗策略，以防止肝纤维化。

“目前，肝纤维化的治疗选择是有限的，不能治愈，说：”研究的高级作者斯特凡·维尔茨弗里德里希 - 亚历山大大学埃尔兰根 - 纽伦堡。 “我们确定了新的免疫因素，有助于肝纤维化的发展，开辟了新的途径，为治疗这种病情严重。”

肝纤维化指的是细胞外基质（ECM）蛋白的有害沉积物的积累，它可能最终导致器官功能衰竭。过去的研究已经表明，这种损害是在肝脏异常的免疫反应，但很少被称为纤维化的分子和细胞。

Wirtz和他的团队在新的研究中，发现血液中的IL-33的量明显高于正常的肝病患者。在此观察，他们发现，注射到小鼠体内，引起ECM蛋白积聚在肝脏，IL-33，，而缺乏IL-33转基因小鼠在很大程度上纤维化保护。研究人员还确定免疫​​网络相关IL-33的有害影响，并发现，这种分子激活免疫细胞，称为2型先天性淋巴的细胞（ILC2），以前从未与肝病。

“我们的研究结果表明IL-33作为一种新型的生物标志物，可能导致纤维化患者的早期发现，这可能是非常有价值的，以防止进一步损害肝脏，”维尔茨说。 “此外，研究表明，IL-33或ILC2反应​​靶向药物可能是一种很有前途的战略，以防止肝纤维化和慢性肝病。”


免疫，Mchedlidze等。：“白细胞介素-33-依赖先天淋巴细胞介导肝纤维化。” 10.1016/j.immuni.2013.07.018

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