Complement system activation in ANCA vasculitis: A translational success story?
The ANCA-associated vasculitides (AAV) are characterized by pauci-immune necrotizing small to medium size vessel vasculitis frequently including necrotizing crescentric glomerulonephritis. Neutrophil activation by ANCA appears a primary pathogenic event. More recently, the complement system has been...
Ausführliche Beschreibung
Autor*in: |
Kallenberg, Cees G.M. [verfasserIn] |
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Format: |
E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2015transfer abstract |
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Umfang: |
4 |
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Übergeordnetes Werk: |
Enthalten in: Letter regarding the article: Changes in BNP and cardiac troponin I after high-intensity interval and endurance exercise in heart failure patients and healthy controls - Gayda, Mathieu ELSEVIER, 2015, Amsterdam [u.a.] |
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Übergeordnetes Werk: |
volume:68 ; year:2015 ; number:1 ; pages:53-56 ; extent:4 |
Links: |
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DOI / URN: |
10.1016/j.molimm.2015.06.005 |
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ELV023269537 |
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520 | |a The ANCA-associated vasculitides (AAV) are characterized by pauci-immune necrotizing small to medium size vessel vasculitis frequently including necrotizing crescentric glomerulonephritis. Neutrophil activation by ANCA appears a primary pathogenic event. More recently, the complement system has been shown to be involved as well. Activation of the alternative pathway of complement, at least in part via activated neutrophils, results, amongst others, in the generation of C5a, a strong chemoattractant for neutrophils. C5a is also effective in neutrophil priming, a process leading to surface expression of the ANCA antigens so enabling neutrophils to be further activated by ANCA. Both in vitro and in vivo experimental data and histopathological studies from AAV patients underscore the role of complement, and particularly of C5a, in the pathophysiology of AAV. Preliminary data show that blocking of the C5a-receptor is a promising approach in the treatment of AAV. | ||
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10.1016/j.molimm.2015.06.005 doi GBVA2015003000016.pica (DE-627)ELV023269537 (ELSEVIER)S0161-5890(15)00429-0 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 610 VZ 630 640 610 VZ Kallenberg, Cees G.M. verfasserin aut Complement system activation in ANCA vasculitis: A translational success story? 2015transfer abstract 4 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The ANCA-associated vasculitides (AAV) are characterized by pauci-immune necrotizing small to medium size vessel vasculitis frequently including necrotizing crescentric glomerulonephritis. Neutrophil activation by ANCA appears a primary pathogenic event. More recently, the complement system has been shown to be involved as well. Activation of the alternative pathway of complement, at least in part via activated neutrophils, results, amongst others, in the generation of C5a, a strong chemoattractant for neutrophils. C5a is also effective in neutrophil priming, a process leading to surface expression of the ANCA antigens so enabling neutrophils to be further activated by ANCA. Both in vitro and in vivo experimental data and histopathological studies from AAV patients underscore the role of complement, and particularly of C5a, in the pathophysiology of AAV. Preliminary data show that blocking of the C5a-receptor is a promising approach in the treatment of AAV. The ANCA-associated vasculitides (AAV) are characterized by pauci-immune necrotizing small to medium size vessel vasculitis frequently including necrotizing crescentric glomerulonephritis. Neutrophil activation by ANCA appears a primary pathogenic event. More recently, the complement system has been shown to be involved as well. Activation of the alternative pathway of complement, at least in part via activated neutrophils, results, amongst others, in the generation of C5a, a strong chemoattractant for neutrophils. C5a is also effective in neutrophil priming, a process leading to surface expression of the ANCA antigens so enabling neutrophils to be further activated by ANCA. Both in vitro and in vivo experimental data and histopathological studies from AAV patients underscore the role of complement, and particularly of C5a, in the pathophysiology of AAV. Preliminary data show that blocking of the C5a-receptor is a promising approach in the treatment of AAV. complement Elsevier ANCA-associated vasculitis Elsevier C5a Elsevier Heeringa, Peter oth Enthalten in Elsevier Gayda, Mathieu ELSEVIER Letter regarding the article: Changes in BNP and cardiac troponin I after high-intensity interval and endurance exercise in heart failure patients and healthy controls 2015 Amsterdam [u.a.] (DE-627)ELV012849286 volume:68 year:2015 number:1 pages:53-56 extent:4 https://doi.org/10.1016/j.molimm.2015.06.005 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_40 GBV_ILN_227 GBV_ILN_674 AR 68 2015 1 53-56 4 045F 570 |
spelling |
10.1016/j.molimm.2015.06.005 doi GBVA2015003000016.pica (DE-627)ELV023269537 (ELSEVIER)S0161-5890(15)00429-0 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 610 VZ 630 640 610 VZ Kallenberg, Cees G.M. verfasserin aut Complement system activation in ANCA vasculitis: A translational success story? 2015transfer abstract 4 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The ANCA-associated vasculitides (AAV) are characterized by pauci-immune necrotizing small to medium size vessel vasculitis frequently including necrotizing crescentric glomerulonephritis. Neutrophil activation by ANCA appears a primary pathogenic event. More recently, the complement system has been shown to be involved as well. Activation of the alternative pathway of complement, at least in part via activated neutrophils, results, amongst others, in the generation of C5a, a strong chemoattractant for neutrophils. C5a is also effective in neutrophil priming, a process leading to surface expression of the ANCA antigens so enabling neutrophils to be further activated by ANCA. Both in vitro and in vivo experimental data and histopathological studies from AAV patients underscore the role of complement, and particularly of C5a, in the pathophysiology of AAV. Preliminary data show that blocking of the C5a-receptor is a promising approach in the treatment of AAV. The ANCA-associated vasculitides (AAV) are characterized by pauci-immune necrotizing small to medium size vessel vasculitis frequently including necrotizing crescentric glomerulonephritis. Neutrophil activation by ANCA appears a primary pathogenic event. More recently, the complement system has been shown to be involved as well. Activation of the alternative pathway of complement, at least in part via activated neutrophils, results, amongst others, in the generation of C5a, a strong chemoattractant for neutrophils. C5a is also effective in neutrophil priming, a process leading to surface expression of the ANCA antigens so enabling neutrophils to be further activated by ANCA. Both in vitro and in vivo experimental data and histopathological studies from AAV patients underscore the role of complement, and particularly of C5a, in the pathophysiology of AAV. Preliminary data show that blocking of the C5a-receptor is a promising approach in the treatment of AAV. complement Elsevier ANCA-associated vasculitis Elsevier C5a Elsevier Heeringa, Peter oth Enthalten in Elsevier Gayda, Mathieu ELSEVIER Letter regarding the article: Changes in BNP and cardiac troponin I after high-intensity interval and endurance exercise in heart failure patients and healthy controls 2015 Amsterdam [u.a.] (DE-627)ELV012849286 volume:68 year:2015 number:1 pages:53-56 extent:4 https://doi.org/10.1016/j.molimm.2015.06.005 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_40 GBV_ILN_227 GBV_ILN_674 AR 68 2015 1 53-56 4 045F 570 |
allfields_unstemmed |
10.1016/j.molimm.2015.06.005 doi GBVA2015003000016.pica (DE-627)ELV023269537 (ELSEVIER)S0161-5890(15)00429-0 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 610 VZ 630 640 610 VZ Kallenberg, Cees G.M. verfasserin aut Complement system activation in ANCA vasculitis: A translational success story? 2015transfer abstract 4 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The ANCA-associated vasculitides (AAV) are characterized by pauci-immune necrotizing small to medium size vessel vasculitis frequently including necrotizing crescentric glomerulonephritis. Neutrophil activation by ANCA appears a primary pathogenic event. More recently, the complement system has been shown to be involved as well. Activation of the alternative pathway of complement, at least in part via activated neutrophils, results, amongst others, in the generation of C5a, a strong chemoattractant for neutrophils. C5a is also effective in neutrophil priming, a process leading to surface expression of the ANCA antigens so enabling neutrophils to be further activated by ANCA. Both in vitro and in vivo experimental data and histopathological studies from AAV patients underscore the role of complement, and particularly of C5a, in the pathophysiology of AAV. Preliminary data show that blocking of the C5a-receptor is a promising approach in the treatment of AAV. The ANCA-associated vasculitides (AAV) are characterized by pauci-immune necrotizing small to medium size vessel vasculitis frequently including necrotizing crescentric glomerulonephritis. Neutrophil activation by ANCA appears a primary pathogenic event. More recently, the complement system has been shown to be involved as well. Activation of the alternative pathway of complement, at least in part via activated neutrophils, results, amongst others, in the generation of C5a, a strong chemoattractant for neutrophils. C5a is also effective in neutrophil priming, a process leading to surface expression of the ANCA antigens so enabling neutrophils to be further activated by ANCA. Both in vitro and in vivo experimental data and histopathological studies from AAV patients underscore the role of complement, and particularly of C5a, in the pathophysiology of AAV. Preliminary data show that blocking of the C5a-receptor is a promising approach in the treatment of AAV. complement Elsevier ANCA-associated vasculitis Elsevier C5a Elsevier Heeringa, Peter oth Enthalten in Elsevier Gayda, Mathieu ELSEVIER Letter regarding the article: Changes in BNP and cardiac troponin I after high-intensity interval and endurance exercise in heart failure patients and healthy controls 2015 Amsterdam [u.a.] (DE-627)ELV012849286 volume:68 year:2015 number:1 pages:53-56 extent:4 https://doi.org/10.1016/j.molimm.2015.06.005 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_40 GBV_ILN_227 GBV_ILN_674 AR 68 2015 1 53-56 4 045F 570 |
allfieldsGer |
10.1016/j.molimm.2015.06.005 doi GBVA2015003000016.pica (DE-627)ELV023269537 (ELSEVIER)S0161-5890(15)00429-0 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 610 VZ 630 640 610 VZ Kallenberg, Cees G.M. verfasserin aut Complement system activation in ANCA vasculitis: A translational success story? 2015transfer abstract 4 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The ANCA-associated vasculitides (AAV) are characterized by pauci-immune necrotizing small to medium size vessel vasculitis frequently including necrotizing crescentric glomerulonephritis. Neutrophil activation by ANCA appears a primary pathogenic event. More recently, the complement system has been shown to be involved as well. Activation of the alternative pathway of complement, at least in part via activated neutrophils, results, amongst others, in the generation of C5a, a strong chemoattractant for neutrophils. C5a is also effective in neutrophil priming, a process leading to surface expression of the ANCA antigens so enabling neutrophils to be further activated by ANCA. Both in vitro and in vivo experimental data and histopathological studies from AAV patients underscore the role of complement, and particularly of C5a, in the pathophysiology of AAV. Preliminary data show that blocking of the C5a-receptor is a promising approach in the treatment of AAV. The ANCA-associated vasculitides (AAV) are characterized by pauci-immune necrotizing small to medium size vessel vasculitis frequently including necrotizing crescentric glomerulonephritis. Neutrophil activation by ANCA appears a primary pathogenic event. More recently, the complement system has been shown to be involved as well. Activation of the alternative pathway of complement, at least in part via activated neutrophils, results, amongst others, in the generation of C5a, a strong chemoattractant for neutrophils. C5a is also effective in neutrophil priming, a process leading to surface expression of the ANCA antigens so enabling neutrophils to be further activated by ANCA. Both in vitro and in vivo experimental data and histopathological studies from AAV patients underscore the role of complement, and particularly of C5a, in the pathophysiology of AAV. Preliminary data show that blocking of the C5a-receptor is a promising approach in the treatment of AAV. complement Elsevier ANCA-associated vasculitis Elsevier C5a Elsevier Heeringa, Peter oth Enthalten in Elsevier Gayda, Mathieu ELSEVIER Letter regarding the article: Changes in BNP and cardiac troponin I after high-intensity interval and endurance exercise in heart failure patients and healthy controls 2015 Amsterdam [u.a.] (DE-627)ELV012849286 volume:68 year:2015 number:1 pages:53-56 extent:4 https://doi.org/10.1016/j.molimm.2015.06.005 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_40 GBV_ILN_227 GBV_ILN_674 AR 68 2015 1 53-56 4 045F 570 |
allfieldsSound |
10.1016/j.molimm.2015.06.005 doi GBVA2015003000016.pica (DE-627)ELV023269537 (ELSEVIER)S0161-5890(15)00429-0 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 610 VZ 630 640 610 VZ Kallenberg, Cees G.M. verfasserin aut Complement system activation in ANCA vasculitis: A translational success story? 2015transfer abstract 4 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The ANCA-associated vasculitides (AAV) are characterized by pauci-immune necrotizing small to medium size vessel vasculitis frequently including necrotizing crescentric glomerulonephritis. Neutrophil activation by ANCA appears a primary pathogenic event. More recently, the complement system has been shown to be involved as well. Activation of the alternative pathway of complement, at least in part via activated neutrophils, results, amongst others, in the generation of C5a, a strong chemoattractant for neutrophils. C5a is also effective in neutrophil priming, a process leading to surface expression of the ANCA antigens so enabling neutrophils to be further activated by ANCA. Both in vitro and in vivo experimental data and histopathological studies from AAV patients underscore the role of complement, and particularly of C5a, in the pathophysiology of AAV. Preliminary data show that blocking of the C5a-receptor is a promising approach in the treatment of AAV. The ANCA-associated vasculitides (AAV) are characterized by pauci-immune necrotizing small to medium size vessel vasculitis frequently including necrotizing crescentric glomerulonephritis. Neutrophil activation by ANCA appears a primary pathogenic event. More recently, the complement system has been shown to be involved as well. Activation of the alternative pathway of complement, at least in part via activated neutrophils, results, amongst others, in the generation of C5a, a strong chemoattractant for neutrophils. C5a is also effective in neutrophil priming, a process leading to surface expression of the ANCA antigens so enabling neutrophils to be further activated by ANCA. Both in vitro and in vivo experimental data and histopathological studies from AAV patients underscore the role of complement, and particularly of C5a, in the pathophysiology of AAV. Preliminary data show that blocking of the C5a-receptor is a promising approach in the treatment of AAV. complement Elsevier ANCA-associated vasculitis Elsevier C5a Elsevier Heeringa, Peter oth Enthalten in Elsevier Gayda, Mathieu ELSEVIER Letter regarding the article: Changes in BNP and cardiac troponin I after high-intensity interval and endurance exercise in heart failure patients and healthy controls 2015 Amsterdam [u.a.] (DE-627)ELV012849286 volume:68 year:2015 number:1 pages:53-56 extent:4 https://doi.org/10.1016/j.molimm.2015.06.005 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_40 GBV_ILN_227 GBV_ILN_674 AR 68 2015 1 53-56 4 045F 570 |
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author |
Kallenberg, Cees G.M. |
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Kallenberg, Cees G.M. ddc 570 ddc 610 ddc 630 Elsevier complement Elsevier ANCA-associated vasculitis Elsevier C5a Complement system activation in ANCA vasculitis: A translational success story? |
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Letter regarding the article: Changes in BNP and cardiac troponin I after high-intensity interval and endurance exercise in heart failure patients and healthy controls |
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Letter regarding the article: Changes in BNP and cardiac troponin I after high-intensity interval and endurance exercise in heart failure patients and healthy controls |
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Complement system activation in ANCA vasculitis: A translational success story? |
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Complement system activation in ANCA vasculitis: A translational success story? |
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Complement system activation in ANCA vasculitis: A translational success story? |
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The ANCA-associated vasculitides (AAV) are characterized by pauci-immune necrotizing small to medium size vessel vasculitis frequently including necrotizing crescentric glomerulonephritis. Neutrophil activation by ANCA appears a primary pathogenic event. More recently, the complement system has been shown to be involved as well. Activation of the alternative pathway of complement, at least in part via activated neutrophils, results, amongst others, in the generation of C5a, a strong chemoattractant for neutrophils. C5a is also effective in neutrophil priming, a process leading to surface expression of the ANCA antigens so enabling neutrophils to be further activated by ANCA. Both in vitro and in vivo experimental data and histopathological studies from AAV patients underscore the role of complement, and particularly of C5a, in the pathophysiology of AAV. Preliminary data show that blocking of the C5a-receptor is a promising approach in the treatment of AAV. |
abstractGer |
The ANCA-associated vasculitides (AAV) are characterized by pauci-immune necrotizing small to medium size vessel vasculitis frequently including necrotizing crescentric glomerulonephritis. Neutrophil activation by ANCA appears a primary pathogenic event. More recently, the complement system has been shown to be involved as well. Activation of the alternative pathway of complement, at least in part via activated neutrophils, results, amongst others, in the generation of C5a, a strong chemoattractant for neutrophils. C5a is also effective in neutrophil priming, a process leading to surface expression of the ANCA antigens so enabling neutrophils to be further activated by ANCA. Both in vitro and in vivo experimental data and histopathological studies from AAV patients underscore the role of complement, and particularly of C5a, in the pathophysiology of AAV. Preliminary data show that blocking of the C5a-receptor is a promising approach in the treatment of AAV. |
abstract_unstemmed |
The ANCA-associated vasculitides (AAV) are characterized by pauci-immune necrotizing small to medium size vessel vasculitis frequently including necrotizing crescentric glomerulonephritis. Neutrophil activation by ANCA appears a primary pathogenic event. More recently, the complement system has been shown to be involved as well. Activation of the alternative pathway of complement, at least in part via activated neutrophils, results, amongst others, in the generation of C5a, a strong chemoattractant for neutrophils. C5a is also effective in neutrophil priming, a process leading to surface expression of the ANCA antigens so enabling neutrophils to be further activated by ANCA. Both in vitro and in vivo experimental data and histopathological studies from AAV patients underscore the role of complement, and particularly of C5a, in the pathophysiology of AAV. Preliminary data show that blocking of the C5a-receptor is a promising approach in the treatment of AAV. |
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Complement system activation in ANCA vasculitis: A translational success story? |
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