非小细胞肺癌患者高温射频治疗前、后免疫功能的变化

目的 研究非小细胞肺癌（NSCLC）患者高温射频（RFA）治疗前、后机体免疫功能的变化。方法 CT引导下经皮肺穿刺可伸展锚状电极配合RF－2000射频治疗仪高温射频消融，治疗NSLC患者30例。采用流式细胞术及双抗体夹心法，检测治疗前、后外周血T细胞亚群（CD3^ 、CD4^ 、CD8^ )、NK细胞的百分率及sIL-2R含量的变化。采用LDH释放法检测NK细胞的杀伤活性。结果 治疗前NSCLC患者外周血中CD3^ 、CD4^ 细胞的百分率及CD4^ /CD8^ 细胞的比值降低，NK细胞的百分率和NK细胞杀伤活性亦降低，与对照组相比较差异显著（P＜0．01）。CD8^ 细胞的百分率及sIL-2R含量明显高于正常对照组（P＜0．01），提示患者处于免疫抑制状态。治疗后免疫抑制减轻，CD3^ 、CD4^ 、NK细胞的百分率及CD4^ /CD8^ 细胞的比值明显升高，NK细胞杀伤活性也升高，而CD8^ 细胞的百分率及sIL-2R的含量明显降低，治疗前、后相比较差别明显（P＜0．01）。结论 锚状电极高温射频消融具有免疫激活作用，可使机体的免疫功能得到一定程度的改善。

Changes in the immune function of patients with non-small cell lung cancer before and after radio frequency ablation

Aim To study the changes in the immune function of patients with non-small cell lung cancer(NSCLC) before and after radio frequency ablation(RFA). Methods 30 cases of NSCLC patients were treated by using computer tomograph-guided anchor-shaped electrodes in combination with RF-2000 radio frequency instrument for therapy. Flow cytometry(FCM) was used to detect the changes in percentages of T-lymphocyte subsets(CD3+?CD4+?CD8+),NK cells and the contents of soluble interleukin-2 receptor (sIL-2R) were detected by double sandwich ELISA before and after RFA. LDH enzyme-release assay was used to detect cytotoxic activity of NK cells. Results Before RFA the percentages of CD3+,CD4+ cells and the ratio of CD4+/CD8+ cells from the patients were significantly lower than those from control group(P<0.01). So were the percentages of NK cells and cytotoxic activity of NK cells. The percentages of CD8+ cells and the contents of sIL-2R from the patients were obviously higher than those from control group (P<0.01). After RFA, the percentages of CD3+,CD4+cells and the ratio of CD4+/CD8+ cells increased significantly(P<0.01);the percentages of NK cells and cytotoxic activity of NK cells were also significantly higher than those from pre-RFA group(P<0.01). compared with pre-RFA group , the percentages of CD8+ cells and the contents of sIL-2R decreased markedly (P<0.01). Conclusion RFA may activate and improve cell-mediated immune function to some exent.