Role of CXCR6/CXCL16 in steatohepatitis

CXCR6/CXCL16 在脂肪性肝炎中的作用

• 批准号: G1100448/1
• 负责人: Richard Parker
• 金额: $ 28.42万
• 依托单位: University of Birmingham
• 依托单位国家: 英国
• 项目类别: Fellowship
• 财政年份: 2011
• 资助国家: 英国
• 起止时间: 2011 至 无数据
• 项目状态: 已结题
• 来源: https://gtr.ukri.org/projects?ref=G1100448%2F1
• 关键词: Role; CXCR6; CXCL16; steatohepatitis

Liver disease is a significant health problem in the UK where rates of liver disease are rising as a consequence of hepatitis C infection, rising rates of alcoholic liver disease (ALD) and a high prevalence of non-alcoholic fatty liver disease (NALFD) a liver disease related to obesity, diabetes and high blood pressure. Despite their different causes most chronic liver diseases arise as a consequence of an inflammatory response to liver injury that causes scarring and destruction of the liver leading to liver failure. The inflammation in the liver is due to white blood cells leaving the bloodstream and entering liver tissue where they can orchestrate liver damage. This process is controlled by numerous molecules in the liver and on white cells that promote their entry and retention in the liver. We propose to focus our research on one of these molecules, a chemokine called CXCL16 and its corresponding receptor on white cells, CXCR6. We have already shown that CXCR6 is concentrated on white cells that cause liver damage and I will now determine precisely what this receptor does and by using recently developed specific inhibitors of CXCR6, elucidate the inflammatory process and investigate new means of treating it.

肝病是英国的一个重要健康问题，由于丙型肝炎感染，酒精性肝病（ALD）的发病率上升以及非酒精性脂肪性肝病（NALFD）的高患病率，肝病与肥胖，糖尿病和高血压有关。尽管它们的原因不同，但大多数慢性肝病是由于对肝损伤的炎症反应引起的，所述肝损伤引起肝脏的瘢痕形成和破坏，从而导致肝功能衰竭。肝脏中的炎症是由于白色血细胞离开血液并进入肝组织，在那里它们可以协调肝损伤。这一过程由肝脏和白色细胞上的许多分子控制，这些分子促进它们进入和保留在肝脏中。我们建议将我们的研究集中在这些分子之一，一种称为CXCL 16的趋化因子及其在白色细胞上的相应受体CXCR 6上。我们已经证明CXCR6集中在导致肝损伤的白色细胞上，现在我将精确地确定这种受体的作用，并通过使用最近开发的CXCR6特异性抑制剂，阐明炎症过程并研究治疗它的新方法。