【摘要翻译】肾细胞癌诱导外周血中前列腺E2（PGE2）和T辅助细胞2型细胞因子（Th2）的产生
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【Title】Renal cell carcinoma induces prostaglandin E2 and T-helper type 2 cytokine production in peripheral blood mononuclear cells.
【Source】Ann Surg Oncol. 2003 May;10(4):455-62. Related Articles, Links
【Author】Smyth GP, Stapleton PP, Barden CB, Mestre JR, Freeman TA, Duff MD, Maddali S, Yan Z, Daly JM.
Department of Surgery, Weill Medical College of Cornell University/New York Presbyterian Hospital, New York, New York, USA.
【Abstract】
BACKGROUND: Patients with renal cell carcinoma (RCC) do not develop an effective antitumor immune response, despite significant infiltration by lymphocytes. Tumor production of immunosuppressive factors may account for this failure. The object of this study was to investigate the production of immunosuppressive mediators, especially prostaglandin E(2) (PGE(2)), by RCC. METHODS: Peripheral blood mononuclear cells (PBMC) were cocultured with conditioned medium (CM) from human RCC cell lines in the presence or absence of NS-398, a selective cyclooxygenase 2 (COX-2) inhibitor. Supernatants were analyzed for levels of PGE(2), interleukin (IL)-10, IL-6, IL-2, interferon-gamma, and IL-12. The effects of RCC CM on PBMC proliferation were also examined. The expression of basal and stimulated COX-2 messenger RNA in the cell lines was assessed by reverse transcriptase-polymerase chain reaction. RESULTS: RCC CM significantly increased PGE(2) production by PBMC. T-helper type 2 (Th2) cytokine production was also significantly increased. Th1 cytokines were unchanged or decreased. RCC CM increased proliferation of PBMC. Coculture with NS-398 reduced PBMC PGE(2) production to below control levels and significantly decreased IL-6 production and PBMC proliferation. NS-398 had no effect on cellular production of IL-10 or Th1 cytokines. CONCLUSIONS: Human RCC inhibits the host antitumor immune response by promoting PGE(2) production and Th2 cytokines in PBMC. Selective inhibition of COX-2 may have a role in abrogating this effect.
【翻译】
肾细胞癌诱导外周血中前列腺E2和T辅助细胞2型细胞因子的产生.
背景:肾细胞癌患者虽然有淋巴细胞的浸润,但并没有产生有效的抗癌免疫反应.肿瘤产生了一些抑制免疫物质可能是这种免疫无应答的原因.我们研究的目的的调查肾细胞癌中抑制免疫的物质,特别是前列腺素E(2).
方法:外周血单核细胞在源于人类肾肿瘤细胞株的条件培养基中进行培植.分为两种情况,一种是有加入选择性环氧化酶抑制剂NS-398,另一种则没有加入.
结果:我们发现在肾肿瘤细胞株的条件培养基中由外周血产生的PGE(2)显著增加,T辅助细胞2型细胞因子也显著增加.而在加入选择性环氧化酶抑制剂NS-398的培养基中 PGE(2)较对照组低,且IL-6 的产生和单核细胞的增生也显著减少.NS-398 对细胞的IL-10 或Th1的产生无明显影响.
结论:人类肾肿瘤细胞促进外周血PGE(2)和Th2的产生,从而抑制了人体抗肿瘤免疫系统.选择性COX-2抑制剂可能在对抗肿瘤的这种反应中发挥一定的作用.
【全文】
http://www.dxy.cn/bbs/user/download/2445814/03%5B1%5D.pdf
【Source】Ann Surg Oncol. 2003 May;10(4):455-62. Related Articles, Links
【Author】Smyth GP, Stapleton PP, Barden CB, Mestre JR, Freeman TA, Duff MD, Maddali S, Yan Z, Daly JM.
Department of Surgery, Weill Medical College of Cornell University/New York Presbyterian Hospital, New York, New York, USA.
【Abstract】
BACKGROUND: Patients with renal cell carcinoma (RCC) do not develop an effective antitumor immune response, despite significant infiltration by lymphocytes. Tumor production of immunosuppressive factors may account for this failure. The object of this study was to investigate the production of immunosuppressive mediators, especially prostaglandin E(2) (PGE(2)), by RCC. METHODS: Peripheral blood mononuclear cells (PBMC) were cocultured with conditioned medium (CM) from human RCC cell lines in the presence or absence of NS-398, a selective cyclooxygenase 2 (COX-2) inhibitor. Supernatants were analyzed for levels of PGE(2), interleukin (IL)-10, IL-6, IL-2, interferon-gamma, and IL-12. The effects of RCC CM on PBMC proliferation were also examined. The expression of basal and stimulated COX-2 messenger RNA in the cell lines was assessed by reverse transcriptase-polymerase chain reaction. RESULTS: RCC CM significantly increased PGE(2) production by PBMC. T-helper type 2 (Th2) cytokine production was also significantly increased. Th1 cytokines were unchanged or decreased. RCC CM increased proliferation of PBMC. Coculture with NS-398 reduced PBMC PGE(2) production to below control levels and significantly decreased IL-6 production and PBMC proliferation. NS-398 had no effect on cellular production of IL-10 or Th1 cytokines. CONCLUSIONS: Human RCC inhibits the host antitumor immune response by promoting PGE(2) production and Th2 cytokines in PBMC. Selective inhibition of COX-2 may have a role in abrogating this effect.
【翻译】
肾细胞癌诱导外周血中前列腺E2和T辅助细胞2型细胞因子的产生.
背景:肾细胞癌患者虽然有淋巴细胞的浸润,但并没有产生有效的抗癌免疫反应.肿瘤产生了一些抑制免疫物质可能是这种免疫无应答的原因.我们研究的目的的调查肾细胞癌中抑制免疫的物质,特别是前列腺素E(2).
方法:外周血单核细胞在源于人类肾肿瘤细胞株的条件培养基中进行培植.分为两种情况,一种是有加入选择性环氧化酶抑制剂NS-398,另一种则没有加入.
结果:我们发现在肾肿瘤细胞株的条件培养基中由外周血产生的PGE(2)显著增加,T辅助细胞2型细胞因子也显著增加.而在加入选择性环氧化酶抑制剂NS-398的培养基中 PGE(2)较对照组低,且IL-6 的产生和单核细胞的增生也显著减少.NS-398 对细胞的IL-10 或Th1的产生无明显影响.
结论:人类肾肿瘤细胞促进外周血PGE(2)和Th2的产生,从而抑制了人体抗肿瘤免疫系统.选择性COX-2抑制剂可能在对抗肿瘤的这种反应中发挥一定的作用.
【全文】
http://www.dxy.cn/bbs/user/download/2445814/03%5B1%5D.pdf
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