Journal
JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
Volume 21, Issue 8, Pages 1270-1274Publisher
AMER SOC NEPHROLOGY
DOI: 10.1681/ASN.2010030233
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Funding
- Deutsche Forschungsgemeinschaft [AN372/9-12, GRK 1202]
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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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