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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

Origin, homeostasis and function of Langerhans cells and other langerin-expressing dendritic cells

TL;DR: New developments in the understanding of the biology of LCs and other langerin+ DCs are described and the challenges that remain in identifying the role of different DC subsets in tissue immunity are discussed.
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The Sterile Inflammatory Response

TL;DR: This review focuses on a subset of the many sterile stimuli that can induce inflammation-specifically dead cells and a variety of irritant particles, including crystals, minerals, and protein aggregates.
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How Does Proteinuria Cause Progressive Renal Damage

TL;DR: Evidence indicating that proteinuria may accelerate kidney disease progression to end-stage renal failure is reviewed, and proximal tubular cell receptors for uptake of plasma proteins that are under investigation may provide activation signals on excess tubular protein handling.
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The Pathogenesis of Sepsis

TL;DR: Biomarkers may be used to help diagnose patients with sepsis, and they may also help to identify patients who would benefit from immunomodulatory therapies.
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Interleukin 17 Promotes Angiotensin II–Induced Hypertension and Vascular Dysfunction

TL;DR: It is concluded that IL-17 is critical for the maintenance of angiotensin II–induced hypertension and vascular dysfunction and might be a therapeutic target for this widespread disease.
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