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ANCA disease: immunoserology and pathogenesis Alenka Vizjak Institute of Pathology · Faculty of Medicine University of Ljubljana, Ljubljana, Slovenia.

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ANCA disease: immunoserology and pathogenesis

Recurrence of Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis in Appropriately Immunosuppressed Renal Transplant Patients: A Discussion of Two.

Volume 72, Issue 6, Pages (September 2007)

Nat. Rev. Nephrol. doi: /nrneph

Figure 2 Cell-mediated disease mechanisms of lupus nephritis

Nat. Rev. Nephrol. doi: /nrneph

Figure 3 Neutrophils in liver inflammation

Figure 4 Expression of coagulation protease receptors in renal cells

Figure 4 Interactions between adipose, the microbiome and kidney

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Figure 3 Proposed mechanisms underlying the links

Figure 1 Pathways of complement activation

Figure 2 Overview of the complement system

Volume 60, Issue 5, Pages (November 2001)

Figure 1 Mechanism of thrombus formation during ST-segment

Volume 79, Issue 6, Pages (March 2011)

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

Figure 4 Involvement of SEMA4D in the pathogenesis

Figure 2 Expression of complement activation products in renal samples

Nat. Rev. Rheumatol. doi: /nrrheum

Nat. Rev. Nephrol. doi: /nrneph

Figure 2 Three distinct mechanisms of activation of

Coagulation and innate immune responses: can we view them separately?

Nat. Rev. Nephrol. doi: /nrneph

Nat. Rev. Nephrol. doi: /nrneph

Figure 4 Tumour-induced neutrophil extracellular trap

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Figure 2 Prevention of antigen–antibody

Nat. Rev. Nephrol. doi: /nrneph

Figure 4 Post-test probability as a function of pre-test

Figure 2 Initiation, amplification and propagation of coagulation

Figure 1 The coagulation system

Nat. Rev. Nephrol. doi: /nrneph

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Figure 2 Emerging models of antibody-mediated rejection (ABMR) and

Figure 3 Cascade of events leading from AKI to ALI

Nat. Rev. Nephrol. doi: /nrneph

Figure 4 The molecular configuration of the CD20 molecule

Figure 3 Therapeutic intervention in the complement cascade

Figure 4 Cascade system activation on a biomaterial surface

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Figure 1 Mechanisms of neutrophil extracellular trap formation

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during the alloimmune response

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Figure 3 Pathological activation of complement

Figure 3 Biologics that attenuate effector responses in the kidney

Nat. Rev. Nephrol. doi: /nrneph

Nat. Rev. Nephrol. doi: /nrneph

Figure 1 Principal pathogenic mechanisms of

Figure 1 NETosis pathways and potential therapeutic targets

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Figure 1 The major pathways of lipid metabolism

Figure 1 The release of DNA from dead and dying cells

Figure 2 Biologics that target CD4+ T helper (TH)-cell subsets

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ANCA-associated renal vasculitis

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What is myeloperoxidase doing in ANCA-associated glomerulonephritis?

Diagram depicting the pathogenesis of vascular lesions in ANCA vasculitis and GN. The events from left to right occur sequentially at each site of injury,

Figure 1. Initiation of vasculitic lesions in small vessels by ANCA-activating cytokine-primed neutrophils in the wrong place and at the wrong time. Figure.

ANCA-Associated Vasculitis: Core Curriculum 2020

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Nat. Rev. Nephrol. doi:10.1038/nrneph.2017.37 Figure 3 Proposed model for the interaction of anti-neutrophil cytoplasmic antibody (ANCA), neutrophils and complement activation in the pathogenesis of ANCA-associated vasculitis Figure 3 | Proposed model for the interaction of anti-neutrophil cytoplasmic antibody (ANCA), neutrophils and complement activation in the pathogenesis of ANCA-associated vasculitis. Priming of neutrophils by cytokines, such as C5a or tumour necrosis factor, leads to the translocation of ANCA antigens such as myeloperoxidase (MPO) or proteinase-3 (PR3) from the cytoplasm to the cell surface. ANCAs can further activate primed neutrophils to undergo respiratory burst and degranulation, and to release tissue factor (TF)-bearing microparticles and neutrophil extracellular traps (NETs). Neutrophil activation can lead endothelial cell injury, activation of the coagulation system, and activation of the alternative complement pathway via their cell membranes, microparticles and NETs. Activation of the alternative complement pathway and NETs in turn leads to the generation of C5a, which amplifies the inflammatory response through enhanced neutrophil recruitment and priming of neutrophils for ANCA-mediated activation. Chen, M. et al. (2017) Complement in ANCA-associated vasculitis: mechanisms and implications for management Nat. Rev. Nephrol. doi:10.1038/nrneph.2017.37