人thp -1源性巨噬细胞对补体C1q的表达和调控。

D G Walker
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引用次数: 35

摘要

在人单核细胞系THP-1中检测了C1q表达的调控。由于这些细胞可以分化为具有巨噬细胞特性的细胞并诱导表达C1q,因此它们被用作成熟的人单核/巨噬细胞和间接小胶质细胞的模型。干扰素- γ (ifn - γ)和抗炎类固醇药物地塞米松和强的松是C1q产生的强大刺激剂,单独或联合使用。白细胞介素-6 (IL-6)和脂多糖(LPS)也具有显著的刺激活性。肉豆蔻酸佛波酯,一种蛋白激酶C激活剂,降低了C1q的表达。另外还测试了四类药物对C1q分泌的影响。他克林,而不是吲哚美辛、西咪替丁或丙烯茶碱,显示抑制ifn - γ处理的thp -1来源的巨噬细胞分泌C1q的活性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Expression and regulation of complement C1q by human THP-1-derived macrophages.

The regulation of C1q expression was examined in the human monocytic cell line THP-1. Since these cells can be differentiated into cells with macrophage properties and induced to express C1q, they were used as models for mature human monocyte/macrophages and indirectly microglia. Interferon-gamma (IFN-gamma) and the anti-inflammatory steroid agents dexamethasone and prednisone were powerful stimulators of C1q production, alone or in combination. Interleukin-6 (IL-6) and lipopolysaccharide (LPS) also had significant stimulatory activity. Phorbol myristate acetate, a protein kinase C activator, reduced C1q expression. Four additional classes of pharmacological agents were tested for their effect on C1q secretion. Tacrine, but not indomethacin, cimetidine, or propentofylline, showed activity in inhibiting C1q secretion by IFN-gamma treated THP-1-derived macrophages.

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