CD36 regulates macrophage and endothelial cell activation and multinucleate giant cell formation in anti neutrophil cytoplasm antibody vasculitis

Copyright © 2024. Published by Elsevier Inc.

Bibliographische Detailangaben
Veröffentlicht in:Clinical immunology (Orlando, Fla.). - 1999. - 260(2024) vom: 26. März, Seite 109914
1. Verfasser: Zhang, Xiang (VerfasserIn)
Weitere Verfasser: King, Catherine, Dowell, Alexander, Moss, Paul, Harper, Lorraine, Chanouzas, Dimitrios, Ruan, Xiong-Zhong, Salama, Alan David
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2024
Zugriff auf das übergeordnete Werk:Clinical immunology (Orlando, Fla.)
Schlagworte:Journal Article Research Support, Non-U.S. Gov't Anti-neutrophil cytoplasmic antibody-associated vasculitis CD36 Macrophage Macrophage migration inhibitory factor Microvascular endothelial cells Antibodies, Antineutrophil Cytoplasmic
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245 1 0 |a CD36 regulates macrophage and endothelial cell activation and multinucleate giant cell formation in anti neutrophil cytoplasm antibody vasculitis 
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500 |a Date Revised 10.04.2024 
500 |a published: Print-Electronic 
500 |a Citation Status MEDLINE 
520 |a Copyright © 2024. Published by Elsevier Inc. 
520 |a OBJECTIVE: To investigate CD36 in ANCA-associated vasculitis (AAV), a condition characterized by monocyte/macrophage activation and vascular damage 
520 |a METHODS: CD36 expression was assessed in AAV patients and healthy controls (HC). The impact of palmitic acid (PA) stimulation on multinucleate giant cell (MNGC) formation, macrophage, and endothelial cell activation, with or without CD36 knockdown, was examined 
520 |a RESULTS: CD36 was overexpressed on AAV patients' monocytes compared to HC, regardless of disease activity. AAV patients exhibited elevated soluble CD36 levels in serum and plasma and PR3-ANCA patients' monocytes demonstrated increased MNGC formation following PA stimulation compared to HC. PA stimulation of macrophages or endothelial cells resulted in heightened CD36 expression, cell activation, increased macrophage migration inhibitory factor (MIF) production, and c-Myc expression, with attenuation upon CD36 knockdown 
520 |a CONCLUSION: CD36 participates in macrophage and endothelial cell activation and MNGC formation, features of AAV pathogenesis. AAV treatment may involve targeting CD36 or MIF 
650 4 |a Journal Article 
650 4 |a Research Support, Non-U.S. Gov't 
650 4 |a Anti-neutrophil cytoplasmic antibody-associated vasculitis 
650 4 |a CD36 
650 4 |a Macrophage 
650 4 |a Macrophage migration inhibitory factor 
650 4 |a Microvascular endothelial cells 
650 7 |a Antibodies, Antineutrophil Cytoplasmic  |2 NLM 
700 1 |a King, Catherine  |e verfasserin  |4 aut 
700 1 |a Dowell, Alexander  |e verfasserin  |4 aut 
700 1 |a Moss, Paul  |e verfasserin  |4 aut 
700 1 |a Harper, Lorraine  |e verfasserin  |4 aut 
700 1 |a Chanouzas, Dimitrios  |e verfasserin  |4 aut 
700 1 |a Ruan, Xiong-Zhong  |e verfasserin  |4 aut 
700 1 |a Salama, Alan David  |e verfasserin  |4 aut 
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856 4 0 |u http://dx.doi.org/10.1016/j.clim.2024.109914  |3 Volltext 
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