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目的探讨白细胞介素7(IL7)、IL15对肺结核病患者外周血单个核细胞(PBMC)分泌Th1型细胞因子γ干扰素(IFNγ)、肿瘤坏死因子α(TNFα)和Th2型细胞因子IL4、IL10的影响。方法选择2003年1至9月入院的60例肺结核患者和25名健康对照者,用葡聚糖泛影葡胺密度梯度离心法分离PBMC。按加入刺激物的不同,将每份标本分为6组:RPMI1640组、纯化蛋白衍生物(PPD组)、PPD+IL7组、PPD+IL7抗体组、PPD+IL15组、PPD+IL15抗体组。加入相应刺激物后培养72h,收集上清液,采用酶联免疫吸附法(ELISA)检测各组培养上清液中IFNγ、TNFα、IL4、IL10的水平。结果与PPD组相比,加入IL7的患者组PBMC分泌IFNγ和TNFα显著增高,分别为(107±42)～(157±74)ng/L、(460±128)～(887±242)ng/L;显著抑制IL4和IL10的合成,分别为(58±15)～(31±9)ng/L、(153±40)～(112±32)ng/L。健康对照组PBMC分泌IFNγ和TNFα显著增高,分别为(211±57)～(292±92)ng/L、(1203±390)～(1722±503)ng/L;显著抑制IL4和IL10的合成,分别为(43±13)～(36±11)ng/L、(135±37)～(96±36)ng/L。加入IL15患者组PBMC分泌IFNγ和TNFα显著增高,分别为(107±42)～(231±62)ng/L、(460±128)～(843±208)ng/L;显著抑制IL4和IL10的合成,分别为(58±15)～(37±9)ng/L、(153±40)～(116±41)ng/L。健康对照组PBMC分泌IFNγ和TNFα显著增高,分别为(211±57)～(343±108)ng/L、(1203±390)～(1468±235)ng/L;显著抑制IL4和IL10的合成,分别为(43±13)～(36±8)ng/L、(135±37)～(90±35)ng/L。加入IL7抗体或IL15抗体均可抑制IFNγ和TNFα的分泌,促进IL4和IL10的合成。肺结核患者各组IFNγ、TNFα水平均低于健康对照各组,而IL4、IL10水平比较差异无统计学意义。结论IL7和IL15可作为免疫调节剂,诱导IFNγ及TNFα分泌,抑制IL4及IL10合成,从而调节Th1/Th2平衡,发挥对结核分枝杆菌感染患者的免疫保护作用。
Objective To investigate the effects of interleukin 7 (IL7) and IL15 on the secretion of Th1 cytokin IFNγ, TNFα and Th2 cytokines IL4 and IL10 by peripheral blood mononuclear cells (PBMCs) from patients with pulmonary tuberculosis Impact. Methods Sixty patients with tuberculosis admitted from January to September in 2003 and 25 healthy controls were enrolled. PBMCs were isolated by dextran diatrizoate gradient centrifugation. According to the different stimuli added, each sample was divided into 6 groups: RPMI1640 group, PPD group, PPD + IL7 group, PPD + IL7 antibody group, PPD + IL15 group and PPD + IL15 antibody group. The corresponding stimuli were added and cultured for 72h. The supernatants were collected and the levels of IFNγ, TNFα, IL4 and IL10 in the culture supernatants of each group were detected by enzyme-linked immunosorbent assay (ELISA). Results Compared with PPD group, the levels of IFNγ and TNFα secreted by peripheral blood mononuclear cells were significantly increased in patients with IL7 (107 ± 42) ~ (157 ± 74) ng / L, (460 ± 128) ~ (887 ± 242) ng / L significantly inhibited the synthesis of IL4 and IL10, which were (58 ± 15) ~ (31 ± 9) ng / L and (153 ± 40) ~ (112 ± 32) ng / L, respectively. The levels of IFNγ and TNFα secreted by PBMC in healthy control group were significantly increased from (211 ± 57) to (292 ± 92) ng / L and (1203 ± 390) to (1722 ± 503) ng / L, respectively. (43 ± 13) ~ (36 ± 11) ng / L and (135 ± 37) ~ (96 ± 36) ng / L, respectively. The levels of IFNγ and TNFα secreted by peripheral blood mononuclear cells in IL15 patients were significantly higher (107 ± 42) ~ (231 ± 62) ng / L and (460 ± 128) ~ (843 ± 208) ng / L, (58 ± 15) ~ (37 ± 9) ng / L and (153 ± 40) ~ (116 ± 41) ng / L, respectively. The levels of IFNγ and TNFα secreted by PBMC in healthy control group were significantly higher than that in healthy controls (211 ± 57) ~ (343 ± 108) ng / L and (1203 ± 390) ~ (1468 ± 235) ng / L, respectively. (43 ± 13) ~ (36 ± 8) ng / L, (135 ± 37) ~ (90 ± 35) ng / L, respectively. IL7 antibody or IL15 antibody can inhibit the secretion of IFNγ and TNFα, and promote IL4 and IL10 synthesis. Tuberculosis patients IFNγ, TNFα levels were lower than the healthy control groups, while IL4, IL10 levels were no significant difference. Conclusion IL7 and IL15 can be used as immunomodulatory agents to induce the secretion of IFNγ and TNFα, inhibit the synthesis of IL4 and IL10, and thus regulate the balance of Th1 / Th2 and play an immunoprotective role in patients with Mycobacterium tuberculosis infection.