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Title: | Animal Models of ANCA Associated Vasculitis. | Authors: | Shochet L.;Kitching A.R. ;Holdsworth S. | Monash Health Department(s): | Paediatric - Nephrology Nephrology Immunology and Allergy |
Institution: | (Shochet, Holdsworth, Kitching) Centre for Inflammatory Diseases, Monash University, Department of Medicine, Monash Medical Centre, Clayton, VIC, Australia (Shochet, Holdsworth, Kitching) Department of Nephrology, Monash Health, Clayton, VIC, Australia (Holdsworth) Department of Immunology, Monash Health, Clayton, VIC, Australia (Kitching) Department of Pediatric Nephrology, Monash Health, Clayton, VIC, Australia | Issue Date: | 6-May-2020 | Copyright year: | 2020 | Publisher: | Frontiers Media S.A. (E-mail: info@frontiersin.org) | Place of publication: | Switzerland | Publication information: | Frontiers in Immunology. 11 (no pagination), 2020. Article Number: 525. Date of Publication: 09 Apr 2020. | Journal: | Frontiers in Immunology | Abstract: | Anti-neutrophil cytoplasmic antibody (ANCA) associated vasculitis (AAV) is a rare and severe autoimmune multisystemic disease. Its pathogenesis involves multiple arms of the immune system, as well as complex interactions between immune cells and target organs. Experimental animal models of disease can provide the crucial link from human disease to translational research into new therapies. This is particularly true in AAV, due to low disease incidence and substantial disease heterogeneity. Animal models allow for controlled environments in which disease mechanisms can be defined, without the clinical confounders of environmental and lifestyle factors. To date, multiple animal models have been developed, each of which shed light on different disease pathways. Results from animal studies of AAV have played a crucial role in enhancing our understanding of disease mechanisms, and have provided direction toward newer targeted therapies. This review will summarize our understanding of AAV pathogenesis as has been gleaned from currently available animal models, as well as address their strengths and limitations. We will also discuss the potential for current and new animal models to further our understanding of this important condition.© Copyright © 2020 Shochet, Holdsworth and Kitching. | DOI: | http://monash.idm.oclc.org/login?url=http://dx.doi.org/10.3389/fimmu.2020.00525 | PubMed URL: | 32373109 [http://www.ncbi.nlm.nih.gov/pubmed/?term=32373109] | ISSN: | 1664-3224 (electronic) | URI: | https://repository.monashhealth.org/monashhealthjspui/handle/1/28892 | Type: | Review | Subjects: | pathogenicity protein expression pulmonary vasculitis regulatory T lymphocyte spleen cell Th17 cell CD18 antigen colony stimulating factor complement component C5a receptor CXCL1 chemokine CXCL2 chemokine endothelial leukocyte adhesion molecule 1 immunoglobulin G interleukin 17 interleukin 8 lipopolysaccharide lymphocyte function associated antigen 1 lysosome associated membrane protein 2 mannan binding lectin associated serine proteinase neutrophil cytoplasmic antibody phosphatidylinositol 3 kinase gamma toll like receptor 4 tumor necrosis factor MBL associated serine protease 2 T lymphocyte ANCA associated vasculitis antigen antibody complex autoimmunity bone marrow cell CD4+ T lymphocyte CD8+ T lymphocyte endothelium injury extracellular trap glomerulonephritis immune response leukocyte activation |
Type of Clinical Study or Trial: | Review article (e.g. literature review, narrative review) |
Appears in Collections: | Articles |
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