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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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Podocytes Are Nonhematopoietic Professional Antigen-Presenting Cells

TL;DR: This finding suggests that podocytes may act as antigen-presenting cells, taking up and processing antigens to initiate specific T cell responses, similar to professional hematopoietic cells such as dendritic cells or macrophages.
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Toll-like receptor-4: Renal cells and bone marrow cells signal for neutrophil recruitment during pyelonephritis

TL;DR: It is suggested that TLR4 is required on both intrinsic renal cells and bone marrow-derived immune cells for the control of ascending uropathogenic E. coli infection by initiating chemokine-driven renal neutrophil recruitment.
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Circulating CSF-1 Promotes Monocyte and Macrophage Phenotypes that Enhance Lupus Nephritis

TL;DR: It is found that increasing systemic CSF-1 hastened the onset of lupus nephritis in MRL-Fas(lpr) mice and uncovered a multistep CSf-1-dependent systemic mechanism central to lupu nephitis.
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Exclusive CX3CR1 dependence of kidney DCs impacts glomerulonephritis progression

TL;DR: It is demonstrated that cortical and medullary DCs play specialized roles in their respective kidney compartments, and CX3CR1 is identified as a potential therapeutic target in glomerulonephritis that may involve fewer adverse side effects, such as impaired anti-infectious defense or compromised DC functions in other organs.
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Chemokine Receptor CXCR3 Mediates T Cell Recruitment and Tissue Injury in Nephrotoxic Nephritis in Mice

TL;DR: The findings indicate that the ameliorated nephritis in CXCR3-deficient mice is due to impaired renal trafficking of effector T cells rather than their inability to mount an efficient humoral or cellular immune response.
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