目的探讨艾滋病病毒(HIV)感染对外周血肠道归巢CD8+T细胞亚群Tc1、Tc17与肠道归巢Treg平衡的影响。方法选取62例符合诊断标准的无症状HIV感染者:未治疗组31例,治疗组31例,同时选取41例健康对照,采用流式细胞表面及全血胞内细胞因子染色...目的探讨艾滋病病毒(HIV)感染对外周血肠道归巢CD8+T细胞亚群Tc1、Tc17与肠道归巢Treg平衡的影响。方法选取62例符合诊断标准的无症状HIV感染者:未治疗组31例,治疗组31例,同时选取41例健康对照,采用流式细胞表面及全血胞内细胞因子染色方法,使用BD FACSCanto流式细胞仪检测各项指标,FACSDiva软件分析肠道归巢CD8+T细胞亚群Tc1、Tc17与肠道归巢CD4+T细胞亚群Treg之间的比值变化,比较各组之间的差异及与CD4计数、病毒载量之间的相关性。结果 HIV感染后外周血肠道归巢Tc1/Treg比值显著增高(24.68±16.12 vs11.57±4.75,P<0.001),抗病毒治疗可使该比值显著降低至健康对照水平(15.43±13.90 vs 11.57±4.75,P=0.617);而外周血肠道归巢Tc17/Treg比值在HIV感染后则显著降低(0.61±2.44 vs 1.02±0.95,P<0.001),抗病毒治疗不能恢复该比值(0.57±0.78 vs 0.61±2.44,P<0.001),仍显著低于健康对照(0.57±0.78vs 1.02±0.95,P<0.001);相关性分析表明,外周血肠道归巢Tc1/Treg比值与病毒载量负相关(r=-0.633,P<0.001),与CD4计数无相关性,而Tc17/Treg比值则与病毒载量负相关(r=-0.387,P=0.034),与CD4计数正相关(r=0.404,P=0.027)。结论 HIV感染导致外周血肠道归巢T细胞亚群Tc1、Tc17与Treg平衡紊乱,且与疾病进展相关,抗病毒治疗不能完全修复这种平衡失调。展开更多
Background: In coeliac disease (CD) mucosa, the histological lesion is associated with marked infiltration of T helper cell type 1 (Th1) cells. However, the molecular mechanisms which regulate Th1 cell differentiation...Background: In coeliac disease (CD) mucosa, the histological lesion is associated with marked infiltration of T helper cell type 1 (Th1) cells. However, the molecular mechanisms which regulate Th1 cell differentiation in CD mucosa are unknown.Aims: To analyse expression of transcription factors which control the Th1 cell commitment in CD. Patients: Duodenal mucosal samples were taken from untreated CD patients and normal controls. Methods: Interferon γ (IFN-γ ) and interleukin(IL)-4 RNA expression was examined in T lamina propria lymphocytes by quantitative reverse transcription-polymerase chain reaction. T-bet and STAT-4, two Th1 promoting transcription factors, and STAT-6 and GATA-3, transcription factors which govern T helper cell type 2 (Th2) cell polarisation, were examined in duodenal biopsies by western blotting. The effect of gliadin and IFN-γ on expression of T-bet was examined in an ex vivo culture of biopsies taken from normal and treated CD patients. Results: As expected, IFN-γ but not IL-4 RNA transcripts were increased in the mucosa of CD patients in comparison with controls. CD mucosal samples consistently exhibited higher levels of T-bet than controls. However, no difference in active STAT-4 expression was seen between CD patients and controls, suggesting that Th1 polarisation was not induced by local IL-12. GATA-3 and STAT-6 were also low in both CD and control mucosa. In normal duodenal biopsies,IFN-γ stimulated T-bet through a STAT-1 dependent mechanism.Challenge of treated CD but not control biopsies with gliadin enhanced T-bet and this effect was also inhibited by STAT-1 inhibition. Conclusions: This study shows that activation of STAT-1 by IFN-γ promotes T-bet in CD mucosa.展开更多
目的探讨血清细胞因子信号转导负调控因子-3(suppressor of cytokine signaling 3,SOCS-3)、肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)、白细胞介素-16(interleukin-16,IL-16)及T辅助细胞1/T辅助细胞2(Th1/Th2)与妊娠期高血压...目的探讨血清细胞因子信号转导负调控因子-3(suppressor of cytokine signaling 3,SOCS-3)、肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)、白细胞介素-16(interleukin-16,IL-16)及T辅助细胞1/T辅助细胞2(Th1/Th2)与妊娠期高血压疾病(HDCP)的关系。方法选取2014年1月-2016年6月本院妇产科收治的妊娠期高血压疾病患者182例,其中妊娠期高血压组51例,轻度子痫前期组69例,重度子痫前期组62例。另选择同期分娩健康孕妇65例作为对照组。采用ELISA法检测各组孕妇血清SOCS-3、TNF-α、IL-16及Th1/Th2水平,分析重度子痫前期患者不良妊娠结局与各指标的关系。采用Spearman相关分析各组HDCP患者血清SOCS-3水平与TNF-α、IL-16及Th1/Th2的相关性。结果与对照组比较,轻度子痫前期组和重度子痫前期组血清SOCS-3水平均明显降低(0.59±0.12 vs 0.14±0.03和0.08±0.01;P均<0.05)。各组TNF-α、IL-16及Th1/Th2水平均高于对照组,且重度子痫前期组较轻度子痫前期组升高更明显[TNF-α(ng/L):12.58±2.37 vs 34.75±6.42和61.53±9.26;IL-16(ng/L):108.47±35.24 vs 187.63±81.47和284.62±113.58;Th1/Th2:9.27±2.38 vs20.15±4.82和26.48±6.13;P均<0.05]。重度子痫前期患者中,SOCS-3低表达组胎儿宫内窘迫综合征、胎儿生长受限及新生儿窒息的发生率均显著高于高表达组(P均<0.05),TNF-α、IL-16、Th1/Th2高表达组早产及胎儿生长受限的发生率均显著高于低表达组(P均<0.05)。相关分析显示,妊娠期高血压患者血清SOCS-3水平与TNF-α、IL-16、Th1/Th2均呈负相关(r=-0.528,r=-0.506,r=-0.126;P均<0.05)。结论监测孕妇血清SOCS-3、TNF-α、IL-16及Th1/Th2对妊娠期高血压疾病尤其是重度子痫前期的早发现、早诊断、早治疗具有一定的临床指导意义。展开更多
文摘目的探讨艾滋病病毒(HIV)感染对外周血肠道归巢CD8+T细胞亚群Tc1、Tc17与肠道归巢Treg平衡的影响。方法选取62例符合诊断标准的无症状HIV感染者:未治疗组31例,治疗组31例,同时选取41例健康对照,采用流式细胞表面及全血胞内细胞因子染色方法,使用BD FACSCanto流式细胞仪检测各项指标,FACSDiva软件分析肠道归巢CD8+T细胞亚群Tc1、Tc17与肠道归巢CD4+T细胞亚群Treg之间的比值变化,比较各组之间的差异及与CD4计数、病毒载量之间的相关性。结果 HIV感染后外周血肠道归巢Tc1/Treg比值显著增高(24.68±16.12 vs11.57±4.75,P<0.001),抗病毒治疗可使该比值显著降低至健康对照水平(15.43±13.90 vs 11.57±4.75,P=0.617);而外周血肠道归巢Tc17/Treg比值在HIV感染后则显著降低(0.61±2.44 vs 1.02±0.95,P<0.001),抗病毒治疗不能恢复该比值(0.57±0.78 vs 0.61±2.44,P<0.001),仍显著低于健康对照(0.57±0.78vs 1.02±0.95,P<0.001);相关性分析表明,外周血肠道归巢Tc1/Treg比值与病毒载量负相关(r=-0.633,P<0.001),与CD4计数无相关性,而Tc17/Treg比值则与病毒载量负相关(r=-0.387,P=0.034),与CD4计数正相关(r=0.404,P=0.027)。结论 HIV感染导致外周血肠道归巢T细胞亚群Tc1、Tc17与Treg平衡紊乱,且与疾病进展相关,抗病毒治疗不能完全修复这种平衡失调。
文摘Background: In coeliac disease (CD) mucosa, the histological lesion is associated with marked infiltration of T helper cell type 1 (Th1) cells. However, the molecular mechanisms which regulate Th1 cell differentiation in CD mucosa are unknown.Aims: To analyse expression of transcription factors which control the Th1 cell commitment in CD. Patients: Duodenal mucosal samples were taken from untreated CD patients and normal controls. Methods: Interferon γ (IFN-γ ) and interleukin(IL)-4 RNA expression was examined in T lamina propria lymphocytes by quantitative reverse transcription-polymerase chain reaction. T-bet and STAT-4, two Th1 promoting transcription factors, and STAT-6 and GATA-3, transcription factors which govern T helper cell type 2 (Th2) cell polarisation, were examined in duodenal biopsies by western blotting. The effect of gliadin and IFN-γ on expression of T-bet was examined in an ex vivo culture of biopsies taken from normal and treated CD patients. Results: As expected, IFN-γ but not IL-4 RNA transcripts were increased in the mucosa of CD patients in comparison with controls. CD mucosal samples consistently exhibited higher levels of T-bet than controls. However, no difference in active STAT-4 expression was seen between CD patients and controls, suggesting that Th1 polarisation was not induced by local IL-12. GATA-3 and STAT-6 were also low in both CD and control mucosa. In normal duodenal biopsies,IFN-γ stimulated T-bet through a STAT-1 dependent mechanism.Challenge of treated CD but not control biopsies with gliadin enhanced T-bet and this effect was also inhibited by STAT-1 inhibition. Conclusions: This study shows that activation of STAT-1 by IFN-γ promotes T-bet in CD mucosa.
文摘目的探讨血清细胞因子信号转导负调控因子-3(suppressor of cytokine signaling 3,SOCS-3)、肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)、白细胞介素-16(interleukin-16,IL-16)及T辅助细胞1/T辅助细胞2(Th1/Th2)与妊娠期高血压疾病(HDCP)的关系。方法选取2014年1月-2016年6月本院妇产科收治的妊娠期高血压疾病患者182例,其中妊娠期高血压组51例,轻度子痫前期组69例,重度子痫前期组62例。另选择同期分娩健康孕妇65例作为对照组。采用ELISA法检测各组孕妇血清SOCS-3、TNF-α、IL-16及Th1/Th2水平,分析重度子痫前期患者不良妊娠结局与各指标的关系。采用Spearman相关分析各组HDCP患者血清SOCS-3水平与TNF-α、IL-16及Th1/Th2的相关性。结果与对照组比较,轻度子痫前期组和重度子痫前期组血清SOCS-3水平均明显降低(0.59±0.12 vs 0.14±0.03和0.08±0.01;P均<0.05)。各组TNF-α、IL-16及Th1/Th2水平均高于对照组,且重度子痫前期组较轻度子痫前期组升高更明显[TNF-α(ng/L):12.58±2.37 vs 34.75±6.42和61.53±9.26;IL-16(ng/L):108.47±35.24 vs 187.63±81.47和284.62±113.58;Th1/Th2:9.27±2.38 vs20.15±4.82和26.48±6.13;P均<0.05]。重度子痫前期患者中,SOCS-3低表达组胎儿宫内窘迫综合征、胎儿生长受限及新生儿窒息的发生率均显著高于高表达组(P均<0.05),TNF-α、IL-16、Th1/Th2高表达组早产及胎儿生长受限的发生率均显著高于低表达组(P均<0.05)。相关分析显示,妊娠期高血压患者血清SOCS-3水平与TNF-α、IL-16、Th1/Th2均呈负相关(r=-0.528,r=-0.506,r=-0.126;P均<0.05)。结论监测孕妇血清SOCS-3、TNF-α、IL-16及Th1/Th2对妊娠期高血压疾病尤其是重度子痫前期的早发现、早诊断、早治疗具有一定的临床指导意义。
