000K  utf8
1100  $c2018
1500  eng
2050  urn:nbn:de:gbv:8:3-2021-00881-5
2051  10.3389/fimmu.2018.00680
3000  Lamprecht, Peter
3010  Busch, Hauke
3010  Ehlers, Marc
3010  Epplen, Jörg T
3010  Fischer, Nicole
3010  Gemoll, Timo
3010  Hasselbacher, Katrin
3010  Holl-Ulrich, Konstanze
3010  Humrich, Jens Y
3010  Ibrahim, Saleh
3010  Kalies, Kathrin
3010  Karsten, Christian M
3010  Kerstein, Anja
3010  Klapa, Sebastian
3010  Lange, Tanja
3010  Laskay, Tamas
3010  Laudien, Martin
3010  Manz, Rudolf
3010  Müller, Antje
3010  Nieberding, Relana
3010  Petersen, Frank
3010  Pries, Ralph
3010  Riemekasten, Gabriela
3010  Schinke, Susanne
3010  Schumacher, Udo
3010  Ullrich, Sebastian
3010  Weppner, Gesche
3010  Wiech, Thorsten
3010  Yu, Xinhua
4000  Pathogenetic and Clinical Aspects of Anti-Neutrophil Cytoplasmic Autoantibody-Associated Vasculitides  [Lamprecht, Peter]
4209  Anti-neutrophil cytoplasmic autoantibodies (ANCA) targeting proteinase 3 (PR3) and myeloperoxidase expressed by innate immune cells (neutrophils and monocytes) are salient diagnostic and pathogenic features of small vessel vasculitis, comprising granulomatosis with polyangiitis (GPA), microscopic polyangiitis, and eosinophilic GPA. Genetic studies suggest that ANCA-associated vasculitides (AAV) constitute separate diseases, which share common immunological and pathological features, but are otherwise heterogeneous. The successful therapeutic use of anti-CD20 antibodies emphasizes the prominent role of ANCA and possibly other autoantibodies in the pathogenesis of AAV. However, to elucidate causal effects in AAV, a better understanding of the complex interplay leading to the emergence of B lymphocytes that produce pathogenic ANCA remains a challenge. Different scenarios seem possible; e.g., the break of tolerance induced by a shift from non-pathogenic toward pathogenic autoantigen epitopes in inflamed tissue. This review gives a brief overview on current knowledge about genetic and epigenetic factors, barrier dysfunction and chronic non-resolving inflammation, necro-inflammatory auto-amplification of cellular death and inflammation, altered autoantigen presentation, alternative complement pathway activation, alterations within peripheral and inflamed tissue-residing T- and B-cell populations, ectopic lymphoid tissue neoformation, the characterization of PR3-specific T-cells, properties of ANCA, links between autoimmune disease and infection-triggered pathology, and animal models in AAV.
4950  https://doi.org/10.3389/fimmu.2018.00680$xR$3Volltext$534
4950  https://nbn-resolving.org/urn:nbn:de:gbv:8:3-2021-00881-5$xR$3Volltext$534
4961  https://macau.uni-kiel.de/receive/macau_mods_00002297
5051  610
5550  Animals
5550  Antibodies, Antineutrophil Cytoplasmic
5550  Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis
5550  Anti-neutrophil Cytoplasmic Autoantibodies
5550  Anti-neutrophil Cytoplasmic Autoantibody Vasculitides
5550  B-Lymphocytes
5550  Cell Death
5550  Complement Pathway, Alternative
5550  Eosinophilic Granulomatosis With Polyangiitis
5550  Granulomatosis With Polyangiitis
5550  Humans
5550  Immunoglobulin G
5550  Microscopic Polyangiitis