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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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Ferroptosis: A Trigger of Proinflammatory State Progression to Immunogenicity in Necroinflammatory Disease.

TL;DR: Ferroptosis as mentioned in this paper is a newly discovered non-apoptotic form of cell death, characterized by excessive lipid peroxidation and overload iron, which occurs in cancer, neurodegeneration, immune and inflammatory diseases, as well as ischemia/reperfusion injury.
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Small Leucine-Rich Proteoglycans in Renal Inflammation: Two Sides of the Coin.

TL;DR: It is proposed that the dichotomy in SLRP signaling (pro- and anti-inflammatory) allows for fine-tuning the inflammatory response, which is decisive for the outcome of inflammatory kidney diseases.
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Systematic exploration of Astragalus membranaceus and Panax ginseng as immune regulators: Insights from the comparative biological and computational analysis.

TL;DR: A novel comprehensive molecular mechanism analysis method was established and applied to clarify the scientific connotation of AM andPG as immune regulation, with similar herbal tonic effect provided in clinical practice of TCM, which can provide a new line of research for drug development (immune booster) using AM and PG.
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The Changing Landscape of Renal Inflammation

TL;DR: Recent advances in understanding of leukocyte accumulation in the kidney are reviewed, emphasizing key chemokines involved in GN and features of renal inflammation such as the evolving concept of immune cell plasticity are discussed.
References
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Journal ArticleDOI

M-type phospholipase A2 receptor as target antigen in idiopathic membranous nephropathy.

TL;DR: A majority of patients with idiopathic membranous nephropathy have antibodies against a conformation-dependent epitope in PLA(2)R, indicating that PLA( 2)R is a major antigen in this disease.
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Cellular pathophysiology of ischemic acute kidney injury

TL;DR: The major components of this dynamic process, which involves hemodynamic alterations, inflammation, and endothelial and epithelial cell injury, followed by repair that can be adaptive and restore epithelial integrity or maladaptive, leading to chronic kidney disease are reviewed.
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von Willebrand Factor–Cleaving Protease in Thrombotic Thrombocytopenic Purpura and the Hemolytic–Uremic Syndrome

TL;DR: In this article, the authors investigated the prevalence of von Willebrand factor-cleaving protease deficiency in patients with familial and non-familial forms of thrombocytopenic purpura and hemolytic-uremic syndrome.
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Netting neutrophils in autoimmune small-vessel vasculitis.

TL;DR: It is shown that chromatin fibers, so-called neutrophil extracellular traps (NETs), are released by ANCA-stimulated neutrophils and contain the targeted autoantigens proteinase-3 and myeloperoxidase (MPO).
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