TY  - JOUR
N1  - This version is the author accepted manuscript. For information on re-use, please refer to the publisher?s terms and conditions.
JF  - Clinical Immunology
TI  - CD36 regulates macrophage and endothelial cell activation and multinucleate giant cell formation in anti neutrophil cytoplasm antibody vasculitis
PB  - ACADEMIC PRESS INC ELSEVIER SCIENCE
N2  - Objective:
To investigate CD36 in ANCA-associated vasculitis (AAV), a condition characterized by monocyte/macrophage activation and vascular damage.
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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.
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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.
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Conclusion:
CD36 participates in macrophage and endothelial cell activation and MNGC formation, features of AAV pathogenesis. AAV treatment may involve targeting CD36 or MIF.
Y1  - 2024/03//
UR  - http://dx.doi.org/10.1016/j.clim.2024.109914
KW  - CD36; Macrophage migration inhibitory factor; Macrophage; Microvascular
endothelial cells; Anti-neutrophil cytoplasmic antibody-associated vasculitis
EP  - 11
SN  - 1521-6616
A1  - Zhang, Xiang
A1  - King, Catherine
A1  - Dowell, Alexander
A1  - Moss, Paul
A1  - Harper, Lorraine
A1  - Chanouzas, Dimitrios
A1  - Ruan, Xiong-zhong
A1  - Salama, Alan David
AV  - public
VL  - 260
ID  - discovery10193064
ER  -