Renal mesangial cell-macrophage interact

自身免疫性疾病是由人体自身免疫系统引起的疾病。一种这样的疾病是系统性红斑狼疮（SLE），与DNA抗体相关，另一种是系统性血管炎，与称为抗中性粒细胞胞质抗体（ANCA）的白色血细胞抗体相关。这两种疾病都会引起严重的健康问题，如肾衰竭和肺部疾病。然而，为什么某些人发展肾脏问题，而其他人避免它仍然是未知的。我们已经表明，发展肾脏疾病的倾向与循环白色血细胞和肾脏本身细胞上某些蛋白质（受体）的表达有关。此外，这些细胞以复杂的方式相互作用，影响它们促进损伤或诱导组织修复的能力。这些蛋白质在人类疾病中的作用是否与在动物模型中的作用一样重要，从未得到过真正的测试。我希望测试这些特殊的受体蛋白质在SLE和系统性血管炎患者的肾活检以及这些患者的活细胞中的作用。了解决定侵入肾脏的细胞是否会导致损伤或修复的关键机制，应该可以将这些蛋白质开发为新的治疗靶点。

Auto-immune diseases are those caused by the body‘s own immune system. One such disease is systemic lupus erythematosus (SLE), associated with antibodies to DNA, and another is systemic vasculitis associated with antibodies to white blood cells called anti-neutrophil cytoplasm antibody (ANCA). Both diseases cause significant health problems such as kidney failure and lung disease. However, why certain individuals develop kidney problems while others avoid it remains unknown. We have shown that the tendency to develop kidney disease is related to the expression of certain proteins (receptors) on circulating white blood cells and cells found within the kidney itself. Additionally, these cells interact with each other in a complex manner, influencing their ability to promote damage or induce tissue repair. Whether these proteins play as important a role in human disease as they do in animal models has never really been tested. I wish to test the role of these particular receptor proteins in kidney biopsies taken from patients with SLE and systemic vasculitis as well as in living cells from these patients. Understanding the key mechanisms that determine whether cells invading the kidney cause damage or repair, should allow such proteins to be developed as new therapeutic targets.