Response of SCC-12F, a human squamous cell carcinoma cell line, to complement attack
Response of SCC-12F, a human squamous cell carcinoma cell line, to complement attack
复制标题
DOI：
10.1111/1523-1747.ep12276459
复制
发表时间：
1997-07-01
影响因子：
6.5
通讯作者：
Klein, LM
中科院分区：
文献类型：
--
作者：
Whitlow, MB;Klein, LM
我们研究了人鳞状细胞癌细胞系SCC-12F对补体攻击的反应，发现该细胞对补体裂解完全抵抗，在没有裂解的情况下，细胞上有显著的C3沉积和C5b-9沉积，磷脂酰肌醇特异性磷脂酶C(PIPLC)处理细胞去除了脂质连接的补体调节蛋白CD59和衰变加速因子(DAF)，导致细胞上C3b和C5b-9沉积增加，细胞死亡略有增加，补体处理使细胞释放含有末端补体蛋白的膜小泡。补体诱导SCC-12F产生大量的前列腺素F-2α(PGF(2α))。我们得出结论，CD59和DAF在SCC-12F对补体的抵抗中起重要作用，这些细胞产生膜泡和PGF，以响应补体攻击。在没有细胞死亡的情况下，这些反应可能在补体沉积的炎症性皮肤病的发病机制中起重要作用。
We studied the response of a human squamous cell carcinoma cell line, SCC-12F, to human complement attack and found that the cells were completely resistant to complement lysis, In the absence of lysis, there was significant C3 deposition and C5b-9 deposition on the cells, Removal of the lipid-linked complement regulatory proteins CD59 and decay-accelerating factor (DAF) by treatment of the cells with phosphatidylinositol-specific phospholipase C (PIPLC) resulted in increased C3b and C5b-9 deposition on the cells and a slight increase in cell death, Treatment of the cells with complement caused them to release membrane vesicles containing the terminal complement proteins, In addition, complement induced SCC-12F to produce significant amounts of prostaglandin F-2 alpha (PGF(2 alpha)). We conclude that CD59 and DAF are important in the resistance of SCC-12F to complement and that these cells produce membrane vesicles and PGF,, in response to complement attack. These responses, in the absence of cell death, may be important in the pathogenesis of inflammatory skin disease in which complement is deposited.