Anders, Hans-Joachim and Banas, Bernhard and Schloendorff, Detlef (2004) Signaling danger: Toll-like receptors and their potential roles in kidney disease. JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY, 15 (4). pp. 854-867. ISSN 1046-6673, 1533-3450
Full text not available from this repository. (Request a copy)Abstract
Toll-like receptors (TLR) are an emerging family of receptors that recognize pathogen-associated molecular patterns and promote the activation of leukocytes and intrinsic renal cells. Ligands of the TLR include exogenous microbial components such as LPS (TLR4), lipoproteins and peptidoglycans (TLR1, -2, -6), viral RNA (TLR3), bacterial and viral unmethylated cytosin-guanosin dinucleotide (CpG)-DNA (TLR9), and endogenous molecules including heat-shock proteins and extracellular matrix molecules. Upon stimulation, TLR induce expression of inflammatory cytokines or costimulatory molecules via the MyD88-dependent and MyD88-independent signaling pathways shared with the interleukin-1 receptors. TLR are differentially expressed on leukocyte subsets and non-immune cells and appear to regulate important aspects of innate and adaptive immune responses. Tubular epithelial cells are among the non-immune cells that express TLR1, -2, -3, -4, and -6, suggesting that these TLR might contribute to the activation of immune responses in tubulointerstitial injury (e.g., bacterial pyelonephritis, sepsis, and transplant nephropathy). In addition, TLR9 has been shown to be involved in antigen-induced immune complex glomerulonephritis and lupus nephritis by regulating Immoral and cellular immune responses. TLR are evolutionary conserved regulators of innnate and adaptive immune reponses. It is likely that TLR are involved in many if not all types of renal inflammation. Here the authors provide an overview on the biology of TLR, summarize the present data on their expression in the kidney, and provide an outlook for the potential roles of TLR in kidney disease.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | NF-KAPPA-B; SYSTEMIC-LUPUS-ERYTHEMATOSUS; BACTERIAL CPG-DNA; IMMUNE-COMPLEX GLOMERULONEPHRITIS; DENDRITIC CELL MATURATION; TUBULAR EPITHELIAL-CELLS; CHRONIC REJECTION EVENTS; NECROSIS-FACTOR-ALPHA; SURFACTANT PROTEIN-A; DOUBLE-STRANDED-RNA; |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Lehrstuhl für Innere Medizin II |
| Depositing User: | Petra Gürster |
| Date Deposited: | 03 Aug 2021 13:35 |
| Last Modified: | 03 Aug 2021 13:35 |
| URI: | https://pred.uni-regensburg.de/id/eprint/37819 |
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