title: Toll-like receptor expression in patients with renal allograft dysfunction.
abstract: Toll-like receptor (TLR) is known to be a mediator of innate immunity, but recent reports have shown that TLR provides a link to adaptive immunity involved in allograft rejection. To explore the expression patterns in various conditions of renal transplantation, we examined TLR subunit mRNA expressions in renal allograft biopsies of acute rejection (AR; n = 11), chronic rejection (CR; n = 15), chronic cyclosporine nephrotoxicity (CsAN; n = 22), and immunoglobulin A nephropathy (IgAN; n = 9) patients. Control tissues (n = 7) were obtained from normal renal cortical tissue of renal cell carcinoma patients. The diagnosis was made according to the Banff 97 classification. The expressions of TLR 2, 3, 4, and 9 mRNA were analyzed by real-time reverse transcriptase-polymerase chain reaction (RT-PCR) using SYBR green. Statistical analysis was performed using analysis of variance (ANOVA) and the Student t test. TLR 2 and 3 mRNA expressions were not significantly different in any group (P > .05). In contrast, TLR 4 mRNA expression was significantly increased in all allograft groups compared with that of controls, and significantly higher in the CsAN than other transplant groups (P < .05). TLR 9 mRNA expression was up-regulated in CsAN and IgAN compared with AR and CR (P < .05). These results suggested that TLR4 mRNA expression was increased in renal allograft patients with chronic allograft dysfunction. Further studies are needed to correlate TLR subtypes with various causes of graft dysfunction among renal allograft patients.
authors.affiliation: Research Institute for Transplantation and Department of Surgery, Yonsei University College of Medicine, Seoul, Korea.
authors.forename: J
authors.initials: J
authors.lastname: Kwon
authors.forename: J
authors.initials: J
authors.lastname: Park
authors.forename: D
authors.initials: D
authors.lastname: Lee
authors.forename: Y S
authors.initials: YS
authors.lastname: Kim
authors.forename: H J
authors.initials: HJ
authors.lastname: Jeong
mesh_terms: D000208:Acute Disease; D001706:Biopsy; D002908:Chronic Disease; D016572:Cyclosporine / Q000633:toxicity; D017931:DNA Primers; D005786:Gene Expression Regulation; D005922:Glomerulonephritis, IGA / Q000235:genetics; D006084:Graft Rejection / Q000139:chemically induced / Q000235:genetics* / Q000473:pathology; D006801:Humans; D007166:Immunosuppressive Agents / Q000633:toxicity; D016030:Kidney Transplantation / Q000009:adverse effects*; D012333:RNA, Messenger / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction; D051193:Toll-Like Receptors / Q000235:genetics*
chemical_list: D017931:DNA Primers; D007166:Immunosuppressive Agents; D012333:RNA, Messenger; D051193:Toll-Like Receptors; D016572:Cyclosporine