Toll-like receptors and danger signaling in kidney injury.
Why does renal inflammation appear among many of the so-called noninflammatory kidney diseases? Toll-like receptor research provides a surprising answer because activation of the innate immune system involves pathogen-derived as well as nonpathogen-derived immunostimulatory molecules; thus, metabolic, hemodynamic, toxic, or autoimmune forms of tissue damage all can trigger an innate inflammatory response. Because receptor activation is unable to eliminate the underlying drivers of these nonpathogen diseases, it becomes instead a maladaptive pathogenic mechanism that aggravates renal damage. Genetic variants in danger-signaling genes of the innate immune system can also affect individual risk for insufficient pathogen control or exaggerated nonpathogen-related tissue pathology. The evolving concept of danger signaling provides a general mechanism for kidney injury.
Anders
Hans-Joachim
HJ
Department of Nephrology, University of Munich, Munich, Germany. hjanders@med.uni-muenchen.de
D000818:Animals; D006801:Humans; D009393:Nephritis / Q000276:immunology*; D015398:Signal Transduction; D051193:Toll-Like Receptors / Q000502:physiology*
D051193:Toll-Like Receptors