Toll-like receptors: emerging concepts in kidney disease.
OBJECTIVE
To summarize the recent advances in the role of Toll-like receptors (TLRs) in innate immunity, with a special focus on recent studies addressing the expression and function of TLRs in kidney disease.


RESULTS
Pathogen-recognition receptors including TLRs mediate immune activation upon pathogen recognition in different extracellular and intracellular compartments. In contrast to professional antigen-presenting cells, renal cells express a limited pattern of TLR (i.e. express TLR1-TLR6 but lack expression of the endosomal TLR7-TLR9). TLRs on renal cells contribute to the innate immune response in renal infection. Furthermore, recent studies provide experimental evidence for the functional role of TLRs in immune complex disease and autoimmunity. Furthermore, the recognition of endogenous molecules released from injured cells such as biglycan or heat-shock proteins may contribute to acute tubular injury and seem to provide adjuvant activity for renal inflammation. Furthermore, TLR7 and TLR9 are involved in the pathogenesis of lupus nephritis.


CONCLUSIONS
The field of TLR research elucidates the molecular mechanisms of infection-associated kidney diseases but may also further support the concept that innate immunity significantly contributes to the so-called types of nonimmune kidney diseases.
Anders
Hans-Joachim
HJ
Nephrological Center, Medical Policlinic, University of Munich, Munich, Germany.
Schlöndorff
Detlef
D
D000818:Animals; D001424:Bacterial Infections / Q000150:complications* / Q000276:immunology; D003713:Dendritic Cells / Q000276:immunology; D005921:Glomerulonephritis / Q000209:etiology / Q000276:immunology; D006801:Humans; D007113:Immunity, Innate; D007668:Kidney / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D007674:Kidney Diseases / Q000209:etiology / Q000276:immunology; D008024:Ligands; D008181:Lupus Nephritis / Q000209:etiology / Q000276:immunology; D008264:Macrophages / Q000276:immunology; D009393:Nephritis / Q000209:etiology / Q000276:immunology* / Q000378:metabolism / Q000503:physiopathology; D051193:Toll-Like Receptors / Q000276:immunology* / Q000378:metabolism; D014777:Virus Diseases / Q000150:complications* / Q000276:immunology
D008024:Ligands; D051193:Toll-Like Receptors