Abstract
The response to exogenous pathogens leads to activation of innate immunity through the release of pathogen-associated molecular patterns (PAMPs) and their binding to pattern recognition receptors. A classic example is septic shock where Toll receptor 4 recognizes PAMPs. Although well accepted, this concept does not explain the activation of innate immunity and inflammation occurs with transplantation, autoimmunity, or trauma. Increasingly recognized is that endogenous molecules released by dying cells (damage-associated molecular patterns; DAMPs) activate cellular receptors leading to downstream inflammation. Thus endogenous danger signals and exogenous PAMPs elicit similar responses through seemingly similar mechanisms. Also emerging is our understanding that normal repair processes benefit from dampening the immune response to these endogenous danger molecules. Here we focus on the role of DAMPs and their putative receptors in the pathogenesis of acute and chronic kidney diseases.