Toll-like receptors and danger signaling in kidney injury

Journal of the American Society of Nephrology : JASN
Hans-Joachim Anders

Abstract

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.

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Citations

Sep 17, 2013·Nature Reviews. Immunology·Christian KurtsAndrew J Rees
Nov 25, 2011·American Journal of Physiology. Renal Physiology·David P BasileShreevrat Goenka
Dec 12, 2012·The Journal of Clinical Investigation·Shrikant R MulayHans-Joachim Anders
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Sep 22, 2012·Journal of the American Society of Nephrology : JASN·Murthy Narayana DarisipudiHans-Joachim Anders
Jul 17, 2012·Journal of the American Society of Nephrology : JASN·Diane L Rosin, Mark D Okusa
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Jun 28, 2013·International Journal of Molecular Sciences·Santhosh Kumar Vankyala RamaiahHans-Joachim Anders
Aug 26, 2016·American Journal of Physiology. Renal Physiology·Raimund PichlerKatherine R Tuttle

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