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Volume 72, Issue 6, Pages (September 2007)

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Pathogenesis of systemic lupus erythematosus (SLE)

Anifrolumab inhibits cytokine production, plasmacytoid dendritic cell (pDC) activation and the type I (interferon gene signature) IFN gene signature. Anifrolumab.

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Figure 2 Cell-mediated disease mechanisms of lupus nephritis

Nat. Rev. Nephrol. doi: /nrneph

CELL-MEDIATED IMMUNITY

Figure 4 Expression of coagulation protease receptors in renal cells

Figure 4 Interactions between adipose, the microbiome and kidney

Figure 3 Proposed mechanisms underlying the links

Figure 1 Pathways of complement activation

Figure 2 Heat map of targeted therapies in autoimmune diseases

Figure 1 Inducers of the NLRP3 inflammasome related

Figure 3 Putative actions of glucagon-like peptide 1 (GLP-1)

Figure 4 Involvement of SEMA4D in the pathogenesis

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Adaptive Immune System

Figure 2 Expression of complement activation products in renal samples

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Figure 3 Nucleic acid sensors in SLE

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Figure 1 Currently recognized factors that influence the development of scleroderma renal crisis Figure 1 | Currently recognized factors that influence.

Figure 4 Tumour-induced neutrophil extracellular trap

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Figure 3 Molecular mechanisms of crystal-induced necroinflammation

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Figure 2 Molecular pathways involved in the regulation of T-cell differentiation and cytokine production Figure 2 | Molecular pathways involved in the.

Figure 1 Innate immune responses in atherosclerosis

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Inflammation, Autophagy, and Obesity: Common Features in the Pathogenesis of Pancreatitis and Pancreatic Cancer Ilya Gukovsky, Ning Li, Jelena Todoric,

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Figure 3 LDL autoimmunity in atherosclerosis

Figure 4 TNFSF inflammatory activities in tissue cells

during the alloimmune response

Immunity to infectious agents

Figure 3 Pathological activation of complement

Figure 3 Biologics that attenuate effector responses in the kidney

Figure 1 The current model of the pathogenesis of SLE

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Figure 1 NETosis pathways and potential therapeutic targets

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Role of IgE in autoimmunity

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Figure 1 Sequence of events in the development of autoimmune nephritis

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Churg–Strauss syndrome

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Nat. Rev. Nephrol. doi:10.1038/nrneph.2016.71 Figure 3 Neutrophils and NETosis in the pathogenesis of autoimmune and renal diseases Figure 3 | Neutrophils and NETosis in the pathogenesis of autoimmune and renal diseases. Upon exposure to various infectious and 'sterile' stimuli, neutrophils (and low density granulocytes (LDGs) in the setting of systemic lupus erythematosus (SLE)) release neutrophil extracellular traps (NETs). These NETs externalize granular peptides (such as LL-37) in complex with DNA, which, in turn, activate plasmacytoid dendritic cells (pDCs) to synthetize type I interferons (IFN), which have critical roles in SLE pathogenesis. Neutrophils also release inflammatory cytokines that activate T cells and B cells, which produce autoantibodies, potentially contributing to the development of systemic autoimmune and renal diseases. NETs promote the expression of tissue factor, which activates platelets and coagulation factors, thereby promoting thrombosis. This process might contribute to the development of renal diseases, particularly antiphospholipid antibody syndrome (APS) and ANCA-associated vasculitis (AAV). NET-bound proteins, such as metalloproteinases (MMPs) and histones, promote vasculopathy — a feature of renal disease, AAV, SLE and APS — by damaging endothelial cells. Autoantibodies, immune complexes, autoantigens, complement activation factors and cytokines can in turn cause NETosis. NET peptides stimulate NLRP3 inflammasome activation in macrophages, leading to release of IL-1 and IL-18, which promote neutrophil activation and NET formation. Gupta, S. & Kaplan, M. J. (2016) The role of neutrophils and NETosis in autoimmune and renal diseases Nat. Rev. Nephrol. doi:10.1038/nrneph.2016.71