[Toll-like receptors (TLR) in the pathogenesis of kidney diseases].

In the present work general characteristics and occurrence of TLR receptors have been presented. The participation of TLR receptors in kidney pathology in experimental models in the course of urinary system infection, acute renal failure and interstitial fibrosis has been discussed. In addition, the importance of TLRs in various forms of glomerular nephritis and in haemodialytic patients as well as in postrenal-transplant patients has been shown. It is believed that in lipopolysaccharide-induced renal failure in the course of infections caused by Gram negative bacteria TLR4 plays a fundamental role. In the event of damage of renal tubular epithelial cells by mechanical, toxic, or ischemic factors activation of TLRs induces inflammatory processes leading to acute renal failure. In the course of progressive fibrosis of renal interstitial tissue TLR 2 and 4 receptors are stimulated, which results in the fact that immunological and structural cells of renal tissue release chemokines and cytokines, which causes increased inflow of leucocytes and intensification of interstitial nephritis and progressive fibrosis. The study on experimental models on mice MLR (mixed lymphocyte reaction) with genetically conditioned lupus-like disease showed that, CpG-DNA stimulation as a TLR 9 specific agonist intensifies inflammatory symptoms in mice. Similarly in apoferritin induced glomerulopathy (model of immune complex disease) CpG-DNA nucleotide increased glomerulopathy symptoms. It has been proved that activation of mechanisms of inherent immunity through TLR4 receptors affects the frequency and intensity of acute rejections in human organ transplantations. Incidence of acute kidney and lung [transplant rejections was significantly lower in recipients with mutated variants of Toll-like receptor 4 (TLR-4 Asp 299Gly and TLR-4-Tyr399-IIe).