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

Xiang Zhang; Catherine King; Alexander Dowell; Paul Moss; Lorraine Harper; Dimitrios Chanouzas; Xiong-zhong Ruan; Alan David Salama

doi:10.1016/j.clim.2024.109914

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

Xiang Zhang, Catherine King, Alexander Dowell, Paul Moss, Lorraine Harper, Dimitrios Chanouzas, Xiong-zhong Ruan, Alan David Salama^*

^*Corresponding author for this work

Research output: Contribution to journal › Article › peer-review

Abstract

OBJECTIVE: To investigate CD36 in ANCA-associated vasculitis (AAV), a condition characterized by monocyte/macrophage activation and vascular damage.

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.

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.

CONCLUSION: CD36 participates in macrophage and endothelial cell activation and MNGC formation, features of AAV pathogenesis. AAV treatment may involve targeting CD36 or MIF.

Original language	English
Article number	109914
Number of pages	11
Journal	Clinical Immunology
Volume	260
Early online date	27 Jan 2024
DOIs	https://doi.org/10.1016/j.clim.2024.109914
Publication status	Published - Mar 2024

Bibliographical note

Funding:
Funding for the work was from the John F. Moorhead Trust.

Copyright:
© 2024. Published by Elsevier Inc.

Keywords

CD36
Macrophage migration inhibitory factor
Macrophage
Microvascular endothelial cells
Anti-neutrophil cytoplasmic antibodyassociated vasculitis

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Cite this

@article{096f605a71a44e41b075a7e7a40623d9,

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

abstract = "OBJECTIVE: To investigate CD36 in ANCA-associated vasculitis (AAV), a condition characterized by monocyte/macrophage activation and vascular damage.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.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.CONCLUSION: CD36 participates in macrophage and endothelial cell activation and MNGC formation, features of AAV pathogenesis. AAV treatment may involve targeting CD36 or MIF.",

keywords = "CD36, Macrophage migration inhibitory factor, Macrophage, Microvascular endothelial cells, Anti-neutrophil cytoplasmic antibodyassociated vasculitis",

author = "Xiang Zhang and Catherine King and Alexander Dowell and Paul Moss and Lorraine Harper and Dimitrios Chanouzas and Xiong-zhong Ruan and Salama, {Alan David}",

note = "Funding: Funding for the work was from the John F. Moorhead Trust. Copyright: {\textcopyright} 2024. Published by Elsevier Inc.",

year = "2024",

month = mar,

doi = "10.1016/j.clim.2024.109914",

language = "English",

volume = "260",

journal = "Clinical Immunology",

issn = "1521-6616",

publisher = "Elsevier",

}

TY - JOUR

T1 - CD36 regulates macrophage and endothelial cell activation and multinucleate giant cell formation in anti neutrophil cytoplasm antibody vasculitis

AU - Zhang, Xiang

AU - King, Catherine

AU - Dowell, Alexander

AU - Moss, Paul

AU - Harper, Lorraine

AU - Chanouzas, Dimitrios

AU - Ruan, Xiong-zhong

AU - Salama, Alan David

PY - 2024/3

Y1 - 2024/3

N2 - OBJECTIVE: To investigate CD36 in ANCA-associated vasculitis (AAV), a condition characterized by monocyte/macrophage activation and vascular damage.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.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.CONCLUSION: CD36 participates in macrophage and endothelial cell activation and MNGC formation, features of AAV pathogenesis. AAV treatment may involve targeting CD36 or MIF.

AB - OBJECTIVE: To investigate CD36 in ANCA-associated vasculitis (AAV), a condition characterized by monocyte/macrophage activation and vascular damage.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.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.CONCLUSION: CD36 participates in macrophage and endothelial cell activation and MNGC formation, features of AAV pathogenesis. AAV treatment may involve targeting CD36 or MIF.

KW - CD36

KW - Macrophage migration inhibitory factor

KW - Macrophage

KW - Microvascular endothelial cells

KW - Anti-neutrophil cytoplasmic antibodyassociated vasculitis

U2 - 10.1016/j.clim.2024.109914

DO - 10.1016/j.clim.2024.109914

M3 - Article

C2 - 38286173

SN - 1521-6616

VL - 260

JO - Clinical Immunology

JF - Clinical Immunology

M1 - 109914

ER -

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

Abstract

Bibliographical note

Keywords

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Cite this