Costimulation in progressive "non-immune" tubulointerstitial renal disease.

进行性“非免疫”肾小管间质性肾病的共刺激。

• 批准号: nhmrc : 307621
• 负责人: Dr Yiping Wang
• 金额: $ 29万
• 依托单位: The University of Sydney
• 依托单位国家: 澳大利亚
• 项目类别: NHMRC Project Grants
• 财政年份: 2004
• 资助国家: 澳大利亚
• 起止时间: 2004-01-01 至 2006-12-31
• 项目状态: 已结题
• 来源: https://researchdata.edu.au/costimulation-progressive-non-renal-disease/99686
• 关键词: Costimulation; progressive; non; immune; tubulointerstitial

Current treatments for chronic kidney disease are non-specific and frequently ineffective. As a consequence, kidney failure progresses to the stage where patients require dialysis or transplantation to remain alive. Every year about 1700 Australians commence dialysis for this reason and many more die of kidney failure or its complications. This project will examine the role of costimulatory molecules in causing chronic kidney disease (CRD) to progress and their potential as targets for specific therapy to slow the progression of CRD. In chronic kidney diseases of all types, the kidney becomes infiltrated with inflammatory cells. The amount of inflammation has an important bearing on the severity of kidney failure and the rate at which kidney disease progresses. There are a range of different cells that invade the inflamed kidney, some may worsen disease while some may protect against it. Current treatments are non-selective and may, by suppressing inflammation, prevent both repair and protection. Costimulatory molecules have been shown to be important in the regulation of inflammatory cell activation in transplantation and some autoimmune diseases. We, and others, have evidence to suggest that costimulatory molecules may be pivotal to the development and progression of kidney inflammation in CRD as well. This project will use two robust animal models of human CRD to define the role of costimulatory molecules in progression of kidney disease. If, as our preliminary evidence suggests, costimulatory molecules are shown to alter disease progression, then they will provide excellent targets for new treatments. Eventually, treatment directed against costimulatory molecules may be used as more effective and safer therapy for human kidney disease.

目前对慢性肾脏疾病的治疗是非特异性的，并且经常无效。因此，肾衰竭进展到患者需要透析或移植才能存活的阶段。每年约有1700名澳大利亚人因此开始透析，更多的人死于肾衰竭或其并发症。该项目将研究共刺激分子在导致慢性肾脏疾病（CRD）进展中的作用及其作为特异性治疗靶点的潜力，以减缓CRD的进展。在所有类型的慢性肾脏疾病中，肾脏被炎症细胞浸润。炎症的数量对肾衰竭的严重程度和肾脏疾病进展的速度有重要影响。有一系列不同的细胞会入侵发炎的肾脏，有些可能会使疾病恶化，而有些可能会预防疾病。目前的治疗方法是非选择性的，并且可能通过抑制炎症来阻止修复和保护。共刺激分子在移植和一些自身免疫性疾病中对炎症细胞活化的调节起重要作用。我们和其他人有证据表明，共刺激分子可能是关键的发展和进展的肾脏炎症的CRD以及。该项目将使用两种强大的人类CRD动物模型来确定共刺激分子在肾脏疾病进展中的作用。如果，正如我们的初步证据所表明的那样，共刺激分子被证明可以改变疾病的进展，那么它们将为新的治疗提供极好的靶点。最终，针对共刺激分子的治疗可能被用作人类肾脏疾病的更有效和更安全的疗法。