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, metaboli...

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Bibliographic Details
Published inJournal of the American Society of Nephrology Vol. 21; no. 8; pp. 1270 - 1274
Main Author ANDERS, Hans-Joachim
Format Journal Article
LanguageEnglish
Published Washington, DC American Society of Nephrology 01.08.2010
Subjects
Animals
Biological and medical sciences
Humans
Medical sciences
Nephritis - immunology
Nephrology. Urinary tract diseases
Signal Transduction
Toll-Like Receptors - physiology
Signal transduction
Nephrology
Urinary system
Injury
Toll like receptor
Lesion
Kidney
Urology
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Summary: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.
ISSN:1046-6673
1533-3450
DOI:10.1681/asn.2010030233