Increase of IFN-γ and TNF-α production in CD107a + NK-92 cells co-cultured with cervical cancer cell lines pre-treated with the HO-1 inhibitor.
Increase of IFN-γ and TNF-α production in CD107a + NK-92 cells co-cultured with cervical cancer cell lines pre-treated with the HO-1 inhibitor.
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DOI：
10.1186/s12935-014-0100-1
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发表时间：
2014
影响因子：
5.8
通讯作者：
Ortiz-Lazareno PC
中科院分区：
文献类型：
--
作者：
Gómez-Lomelí P;Bravo-Cuellar A;Hernández-Flores G;Jave-Suárez LF;Aguilar-Lemarroy A;Lerma-Díaz JM;Domínguez-Rodríguez JR;Sánchez-Reyes K;Ortiz-Lazareno PC
自然杀伤（NK）细胞通过释放穿孔素和颗粒酶消除病毒感染细胞和肿瘤细胞;它们还产生干扰素γ（IFN-γ）和肿瘤坏死因子α（TNF-α），诱导靶细胞凋亡。许多肿瘤表达血红素加氧酶1（HO-1），这种表达与避免免疫抑制和细胞凋亡有关。在这项工作中，用HO-1抑制剂预处理HO-1+宫颈癌细胞（CCC）系，我们评估了这种抑制是否增强了CCC对NK细胞活性的敏感性。我们通过流式细胞术（FC）评估了HeLa、SiHa和C-33 A CCC中HO-1的表达。CCC用SnPP或ZnPP HO-1抑制剂预处理。然后将NK-92细胞与用HO-1抑制剂预处理或未预处理的HeLa、SiHa和C-33 A CCC共培养，用FC法检测IFN-γ、TNF-α、CD 107 a、Granzyme B、NKp 44、NKp 46、NKp 30和NKG 2D的表达。CCC系HeLa、SiHa和C-33 A表达HO-1。抑制这些细胞中的HO-1可增加CD 107 a + NK-92细胞中IFN-γ和TNF-α的表达。我们观察到与HeLa和SiHa细胞共培养的NK细胞中NKG 2D、NKp 46和NKp 30的表达减少，并且当用HO-1抑制剂预处理HeLa和SiHa细胞时，NK细胞中NKG 2D和NKp 30的表达恢复。我们在与C-33 A细胞共培养的NK细胞中观察到NKp 30表达的类似效应。CCC中HO-1的抑制诱导CD 107 a + NK-92细胞中IFN-γ和TNF-α产生的增加，并恢复NK细胞中NKG 2D、NKp 46和NKp 30的下调。
Natural killer (NK) cells eliminate virus-infected and tumor cells through the release of perforins and granzymes; they also produce Interferon gamma (IFN-γ) and Tumor necrosis factor alpha (TNF-α), which induce apoptosis in target cells. Many tumors express Heme oxygenase 1 (HO-1), and this expression has been associated with avoiding immunosuppression and apoptosis. In this work, HO-1+ Cervical cancer cell (CCC) lines were pre-treated with HO-1 inhibitor and we assessed whether this inhibition enhanced the sensitivity of CCC to NK cell activity. We assessed the expression of HO-1 in HeLa, SiHa, and C-33A CCC by Flow cytometry (FC). CCC were pre-treated with SnPP or ZnPP HO-1 inhibitors. After that, NK-92 cells were co-cultured with HeLa, SiHa, and C-33A CCC pre-treated or not with HO-1 inhibitors, and the expression of IFN-γ, TNF-α, CD107a, Granzyme B, NKp44, NKp46, NKp30, and NKG2D was evaluated by FC. CCC lines HeLa, SiHa, and C-33A expressed HO-1. Inhibition of HO-1 in these cells increased the expression of IFN-γ and TNF-α in CD107a + NK-92 cells. We observed a reduction in the expression of NKG2D, NKp46, and NKp30 in NK cells co-cultured with HeLa and SiHa cells, and when HeLa and SiHa cells were pre-treated with the HO-1 inhibitors, the expression of NKG2D and NKp30 in NK cells was restored. We observed a similar effect in NK cells co-cultured with C-33A cells in NKp30 expression. Inhibition of HO-1 in CCC induces an increase in IFN-γ and TNF-α production in CD107a + NK-92 cells and restores NKG2D, NKp46 and NKp30 downmodulation in NK cells.
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表达NKG2D配体的宫颈癌细胞系能够对NKL细胞上的NKG2D受体调节，具有功能意义。
影响因子：
3
作者：
Jimenez-Perez MI;Jave-Suarez LF;Ortiz-Lazareno PC;Bravo-Cuellar A;Gonzalez-Ramella O;Aguilar-Lemarroy A;Hernandez-Flores G;Pereira-Suarez AL;Daneri-Navarro A;del Toro-Arreola S
通讯作者：
del Toro-Arreola S
影响因子：
11.5
作者：
Berberat, PO;Dambrauskas, Z;Friess, H
通讯作者：
Friess, H
影响因子：
56.9
作者：
Bauer, S;Groh, V;Spies, T
通讯作者：
Spies, T
影响因子：
32.4
作者：
Cosman, D;Müllberg, J;Chalupny, NJ
通讯作者：
Chalupny, NJ
影响因子：
82.9
作者：
Lee, TS;Chau, LY
通讯作者：
Chau, LY