Interleukin 38: Uncoupling Innate Inflammation from Interferons in Lupus

白细胞介素 38：解开狼疮中干扰素引起的先天炎症

• 批准号: nhmrc : 1138791
• 负责人: A/Pr Marcel Nold
• 金额: $ 70.9万
• 依托单位: Monash University
• 依托单位国家: 澳大利亚
• 项目类别: Project Grants
• 财政年份: 2018
• 资助国家: 澳大利亚
• 起止时间: 2018-01-01 至 2021-12-31
• 项目状态: 已结题
• 来源: https://researchdata.edu.au/interleukin-38-uncoupling-interferons-lupus/1318855
• 关键词: Interleukin; 38; Uncoupling; Innate; Inflammation

Systemic lupus erythematosus (SLE) is an incurable autoimmune disease that affects 5 million patients worldwide, mostly young women. Grave multi-organ inflammation and substantial loss of life expectancy render SLE a critical unmet medical need. We found that the immune system protein interleukin 38 disables several signalling pathways essential for SLE progress. We will explore regulation and function of this protein in cells from healthy people and SLE patients and in models of the disease.

系统性红斑狼疮 (SLE) 是一种无法治愈的自身免疫性疾病，影响全球 500 万患者，其中大部分是年轻女性。严重的多器官炎症和预期寿命的大幅丧失使得系统性红斑狼疮成为一个未得到满足的关键医疗需求。我们发现免疫系统蛋白白细胞介素 38 会禁用 SLE 进展所必需的数条信号通路。我们将探索这种蛋白质在健康人和系统性红斑狼疮患者的细胞以及疾病模型中的调节和功能。