Expression and regulation of complement C1q by human THP-1-derived macrophages.
Expression and regulation of complement C1q by human THP-1-derived macrophages.
复制标题
人 THP-1 衍生巨噬细胞对补体 C1q 的表达和调节。
DOI：
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发表时间：
1998
期刊：
影响因子：
--
通讯作者：
D. Walker
中科院分区：
文献类型：
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作者：
D. Walker
在人单核细胞系THP-1中检查C1 q表达的调节。由于这些细胞可以分化成具有巨噬细胞特性的细胞并被诱导表达C1 q，因此它们被用作成熟人单核细胞/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泼尼松是C1 q生产的强大刺激剂，单独或组合。白细胞介素-6（IL-6）和脂多糖（LPS）也具有明显的刺激活性。佛波醇肉豆蔻酸酯，蛋白激酶C激活剂，减少C1 q的表达。测试了另外四类药物对C1 q分泌的影响。他克林，而不是吲哚美辛，西咪替丁，或propentofylline，表现出活性抑制C1 q分泌IFN-γ处理的THP-1衍生的巨噬细胞。
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.
培养的人单核细胞分泌的补体亚成分C1q，其亚基结构与血清C1q相同。
DOI：
10.1042/bj2330451
发表时间：
1986
期刊：
The Biochemical journal
影响因子：
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作者：
Tenner,AJ;Volkin,DB
通讯作者：
Volkin,DB
影响因子：
4.4
作者：
P. Hicks;L. Saunero-Nava;T. D. Du Clos;C. Mold
通讯作者：
P. Hicks;L. Saunero-Nava;T. D. Du Clos;C. Mold
β-淀粉样蛋白通过与 C1q A 链的胶原蛋白样结构域的特定区域结合来激活补体。
DOI：
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发表时间：
1994
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Jiang,H;Burdick,D;Glabe,CG;Cotman,CW;Tenner,AJ
通讯作者：
Tenner,AJ