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The immune system and kidney disease: basic concepts and clinical implications

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TLDR
The kidneys are frequently targeted by pathogenic immune responses against renal autoantigens or by local manifestations of systemic autoimmunity, causing intestinal barrier dysfunction, systemic inflammation and immunodeficiency that contribute to the morbidity and mortality of patients with kidney disease.
Abstract
The kidneys are frequently targeted by pathogenic immune responses against renal autoantigens or by local manifestations of systemic autoimmunity. Recent studies in rodent models and humans have uncovered several underlying mechanisms that can be used to explain the previously enigmatic immunopathology of many kidney diseases. These mechanisms include kidney-specific damage-associated molecular patterns that cause sterile inflammation, the crosstalk between renal dendritic cells and T cells, the development of kidney-targeting autoantibodies and molecular mimicry with microbial pathogens. Conversely, kidney failure affects general immunity, causing intestinal barrier dysfunction, systemic inflammation and immunodeficiency that contribute to the morbidity and mortality of patients with kidney disease. In this Review, we summarize the recent findings regarding the interactions between the kidneys and the immune system.

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References
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Journal ArticleDOI

Proteasomal Processing of Albumin by Renal Dendritic Cells Generates Antigenic Peptides

TL;DR: It is suggested that albumin can be a source of potentially antigenic peptides upon renal injury and that renal DC play a role in processing self-proteins through a proteasome-dependent pathway.
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Systemic Lupus Erythematosus and the Neutrophil

TL;DR: Recent studies implicate a peculiar form of neutrophil death and its extracellular sequelae in mediating inflammation in patients with systemic lupus erythematosus.
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Nephritogenic Potential of Anti-DNA Antibodies against Necrotic Nucleosomes

TL;DR: Exposure to exposed chromatin fragments contain structures that stimulate the innate immune system through Toll-like receptors and the adaptive immune system to produce affinity-maturated pathogenic anti-chromatin and anti-dsDNA antibodies that are central to the development of lupus nephritis.
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