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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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Inflammation in AKI: Current Understanding, Key Questions, and Knowledge Gaps

TL;DR: The most important recent developments in understanding the inflammatory mechanisms of AKI are summarized, key limitations of the commonly used animal models and clinical trial designs that may prevent successful clinical application are highlighted, and priority approaches for research toward clinical translation are suggested.
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Complement in disease: a defence system turning offensive

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References
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TLR4 Promotes Fibrosis but Attenuates Tubular Damage in Progressive Renal Injury

TL;DR: TLR4 attenuates tubular damage but promotes renal fibrosis by modulating the susceptibility of renal cells to TGF-beta, suggesting that TLR4 signaling may be a therapeutic target for the prevention of renal Fibrosis.
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Anti-Neutrophil Cytoplasmic Antibodies and Effector CD4+ Cells Play Nonredundant Roles in Anti-Myeloperoxidase Crescentic Glomerulonephritis

TL;DR: Experimental autoimmune anti-MPO glomerulonephritis was induced by immunizing C57BL/6 mice with human MPO and passive transfer of sera from MPO-immunized Mpo(-/-) mice to LPS-primed mice rapidly induced glomerular neutrophil accumulation and release of MPO, providing in vivo evidence in a relevant vascular bed for both humoral and cellular anti- MPO responses as key inducers of injury.
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Uremic solutes from colon microbes.

TL;DR: There is renewed interest in identifying organic waste solutes that are normally excreted by the kidneys and must be removed by renal replacement therapy when the kidneys fail.
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Aldosterone Promotes Autoimmune Damage by Enhancing Th17-Mediated Immunity

TL;DR: The data suggest that modulation of DC function by aldosterone enhances CD8+ T cell activation and promotes Th17-polarized immune responses, which might contribute to the inflammatory damage leading to hypertension and cardiovascular disease.
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IL-10 Suppresses Chemokines, Inflammation, and Fibrosis in a Model of Chronic Renal Disease

TL;DR: It is concluded that IL-10 blocks inflammation and improves renal function in this model of chronic renal disease and the feasibility of long-term overexpression of a gene using the AAV serotype 1 vector system in a model of renal disease is demonstrated.
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