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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

Renal Dendritic Cells Stimulate IL-10 Production and Attenuate Nephrotoxic Nephritis

TL;DR: It is demonstrated that renal DCs exert a renoprotective effect in nephrotoxic nephritis, possibly by expressing ICOS-L and/or by inducing IL-10 in infiltrating CD4(+) Th1 cells.
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Pathogenesis of the C3 glomerulopathies and reclassification of MPGN

TL;DR: This Review re-examine the previous and current classification schemes of MPGN, focusing on the role of complement, and surveys current data about the pathogenesis of the C3 glomerulopathies, including familial studies and patient cohorts from the USA and Europe.
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Toll-Like Receptors and Danger Signaling in Kidney Injury

TL;DR: Toll-like receptor research provides a surprising answer 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.
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PLA2R Autoantibodies and Recurrent Membranous Nephropathy after Transplantation

TL;DR: Findings regarding a 56-year-old female patient with biopsy-proven membranous nephropathy, a leading cause of the nephrotic syndrome in adults, are reported.
Journal ArticleDOI

High Prevalence of Autoantibodies to hLAMP-2 in Anti–Neutrophil Cytoplasmic Antibody–Associated Vasculitis

TL;DR: In this paper, the involvement of autoantibodies to human lysosome-associated membrane protein-2 (hLAMP-2) in anti-neutrophil cytoplasmic antibody-associated vasculitis is controversial because of the absence of confirmatory data subsequent to the initial reports of their high prevalence in this disease.
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