면역성 신장질환의 유전자 치료 = Gene Therapy for inflammatory renal diseases

다국어 초록 (Multilingual Abstract)

Renal failure caused by a wide variety of etiological factors is characterized by progressive and irreversible deterioration of nephrons in the kidney. Despite the diversity of renal diseases, the appearance of inflammatory cells at the site of tissue injury is the hallmark of almost all renal diseases. Humoral and cell-mediated immune responses and soluble mediators play pivotal roles in the progression of renal injury. The utility of IL-10, a cytokine with potent anti-inflammatory activity, in the treatment of glomerulosclerosis in FGS/Kist mice in which renal disease occurs naturally with agin was studied. The group treated with recombinant anenoviruses encoding IL-10 was shown to have significant suppression of glomerular sclerotic index and reduced proteinuria when compared to LacZ or sham controls. Practical therapies are not currently available, but candidates for molecular therapeutics for renal diseases include vector-based gene therapy and the use of molecular compounds such as anti-inflammatory cytokines. There is a compelling need to improve vector systems, to control transgene expression, and to achieve cell-specific or localized targeting in gene therapy for renal disease.