Impact of chronic IFN-I signalling in liver fibrosis on anti-viral immunity ((2)-P32*)

肝纤维化中慢性 IFN-I 信号传导对抗病毒免疫的影响 ((2)-P32*)

• 批准号: 329565248
• 金额: --
• 依托单位: Institut für Experimentelle Immunologie
• 依托单位国家: 德国
• 项目类别: CRC/Transregios
• 财政年份: 2017
• 资助国家: 德国
• 起止时间: 2016-12-31 至 2019-12-31
• 项目状态: 已结题
• 来源: https://gepris.dfg.de/gepris/projekt/329565248?language=en
• 关键词: Impact; chronic; IFN; signalling; liver

The underlying cellular and molecular factors for the enhanced susceptibility of patients with liver fibrosis to viral and bacterial infections are unclear. Recently, we found that translocation of gut microbiota induces chronic IFN-I expression, which hampers viral clearance in a preliminary experiments. In this project, we aim to explore the cellular and molecular mechanisms by which IFN-I might affect the function of key players of anti-viral immunity i.e. antigen presenting cells, CD4 T and CD8 T cells in liver fibrosis and how this may perpetuate and accelerate the fibrogenic process. The results of this project will enhance our understanding of impaired cellular immunity in patients with liver fibrosis, aggravation of liver fibrosis by persistent infection and potentially open new venues for therapeutic and vaccination approaches.

肝纤维化患者对病毒和细菌感染的易感性增强的潜在细胞和分子因素尚不清楚。最近，我们在初步实验中发现肠道微生物群的易位会诱导慢性 IFN-I 表达，从而阻碍病毒清除。在这个项目中，我们的目标是探索 IFN-I 可能影响抗病毒免疫关键参与者（即肝纤维化中抗原呈递细胞、CD4 T 和 CD8 T 细胞）功能的细胞和分子机制，以及这种机制如何持续和发展。加速纤维化过程。该项目的结果将增强我们对肝纤维化患者细胞免疫受损、持续感染导致肝纤维化加剧的理解，并可能为治疗和疫苗接种方法开辟新的领域。