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 PR3-ANCA patients' monocytes demonstrated increased MNGC formation following PA stimulation compared to MPO-ANCA and 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.

中文翻译：

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CD36在抗中性粒细胞胞质抗体血管炎中调节巨噬细胞和内皮细胞活化以及多核巨细胞形成

客观的

旨在研究 ANCA 相关血管炎 (AAV) 中的 CD36，这是一种以单核细胞/巨噬细胞激活和血管损伤为特征的疾病。

方法

在 AAV 患者和健康对照 (HC) 中评估 CD36 表达。研究了棕榈酸 (PA) 刺激对多核巨细胞 (MNGC) 形成、巨噬细胞和内皮细胞活化的影响，无论是否敲低 CD36。

结果

与 HC 患者相比，无论疾病活动度如何，CD36 在 AAV 患者的单核细胞上过度表达。与 MPO-ANCA 和 HC 相比，AAV 患者血清中可溶性 CD36 水平升高，PR3-ANCA 患者单核细胞在 PA 刺激后 MNGC 形成增加。PA 刺激巨噬细胞或内皮细胞导致 CD36 表达升高、细胞活化、巨噬细胞迁移抑制因子 (MIF) 产生增加和 c-Myc 表达增加，并在 CD36 敲低后减弱。

结论

CD36 参与巨噬细胞和内皮细胞的激活以及 MNGC 的形成，这是 AAV 发病机制的特征。AAV 治疗可能涉及靶向 CD36 或 MIF。