Pathogenetic and Clinical Aspects of Anti-Neutrophil Cytoplasmic Autoantibody-Associated Vasculitides
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Pathogenetic and Clinical Aspects of Anti-Neutrophil Cytoplasmic Autoantibody-Associated Vasculitides. / Lamprecht, Peter; Kerstein, Anja; Klapa, Sebastian; Schinke, Susanne; Karsten, Christian M; Yu, Xinhua; Ehlers, Marc; Epplen, Jörg T; Holl-Ulrich, Konstanze; Wiech, Thorsten; Kalies, Kathrin; Lange, Tanja; Laudien, Martin; Laskay, Tamas; Gemoll, Timo; Schumacher, Udo; Ullrich, Sebastian; Busch, Hauke; Ibrahim, Saleh; Fischer, Nicole; Hasselbacher, Katrin; Pries, Ralph; Petersen, Frank; Weppner, Gesche; Manz, Rudolf; Humrich, Jens Y; Nieberding, Relana; Riemekasten, Gabriela; Müller, Antje.
in: FRONT IMMUNOL, Jahrgang 9, 2018, S. 680.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Review › Forschung
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TY - JOUR
T1 - Pathogenetic and Clinical Aspects of Anti-Neutrophil Cytoplasmic Autoantibody-Associated Vasculitides
AU - Lamprecht, Peter
AU - Kerstein, Anja
AU - Klapa, Sebastian
AU - Schinke, Susanne
AU - Karsten, Christian M
AU - Yu, Xinhua
AU - Ehlers, Marc
AU - Epplen, Jörg T
AU - Holl-Ulrich, Konstanze
AU - Wiech, Thorsten
AU - Kalies, Kathrin
AU - Lange, Tanja
AU - Laudien, Martin
AU - Laskay, Tamas
AU - Gemoll, Timo
AU - Schumacher, Udo
AU - Ullrich, Sebastian
AU - Busch, Hauke
AU - Ibrahim, Saleh
AU - Fischer, Nicole
AU - Hasselbacher, Katrin
AU - Pries, Ralph
AU - Petersen, Frank
AU - Weppner, Gesche
AU - Manz, Rudolf
AU - Humrich, Jens Y
AU - Nieberding, Relana
AU - Riemekasten, Gabriela
AU - Müller, Antje
PY - 2018
Y1 - 2018
N2 - 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.
AB - 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.
KW - Journal Article
KW - Review
U2 - 10.3389/fimmu.2018.00680
DO - 10.3389/fimmu.2018.00680
M3 - SCORING: Review article
C2 - 29686675
VL - 9
SP - 680
JO - FRONT IMMUNOL
JF - FRONT IMMUNOL
SN - 1664-3224
ER -
