Cellular senescence is a signal transduction process which maintained genomic stability and stopped mammalian cell growth. Furthermore, cellular senescence induces a protective response to a variety of DNA damage. How...Cellular senescence is a signal transduction process which maintained genomic stability and stopped mammalian cell growth. Furthermore, cellular senescence induces a protective response to a variety of DNA damage. However, this process is also associated with apoptosis, upregulated secretion of inflammatory cytokine, and promoted surrounding tissue damage. When cellular senescence accumulates to a certain extent, it triggers geriatric diseases, such as chronic inflammation, immune senescence-associated tumors and incontrollable infections. Cellular senescence gene SENEX, which was cloned in 2004, has been demonstrated to play a unique gatekeeper function in human endothelial cells when stress-induced pre-mature senescence and apoptosis occurr. The phenomenon that CD4+CD25+ Treg cells accumulated in the aged population has been well studied in recent years. Now Treg accumulation related to immune-pathology has attracted more interest. CD4+CD25+ Treg did not decline and age, but accumulated and suppressed immunoreaction. The enhanced Treg number and function may be associated with stress-induced premature senescence-mediated unique cellular senescence protection mechanisms, and SENEX may play a critical role in this process. In this article, we summarize the cellular senescence and SENEX gene in the accumulation and functional activity of CD4+CD25+ Treg in the elderly.展开更多
目的探讨参苓白术散对胃癌IV期患者外周血CD4+CD25+Tregs、Foxp3 m RNA及血清细胞因子IL-10、TGF-β1的影响。方法将40例胃癌IV期患者随机分为观察组、对照组各20例。对照组予对症支持治疗,观察组对症支持治疗同时予参苓白术散治疗,治疗...目的探讨参苓白术散对胃癌IV期患者外周血CD4+CD25+Tregs、Foxp3 m RNA及血清细胞因子IL-10、TGF-β1的影响。方法将40例胃癌IV期患者随机分为观察组、对照组各20例。对照组予对症支持治疗,观察组对症支持治疗同时予参苓白术散治疗,治疗4 w后观察两组患者外周血CD4+CD25+Tregs、单核细胞Foxp3 m RNA及血清IL-10、TGF-β1浓度的变化。结果治疗后观察组患者外周血CD4+CD25+Tregs、单核细胞Foxp3 m RNA及血清IL-10、TGF-β1浓度均显著降低(P<0.05),对照组治疗后各项指标无明显变化(P>0.05),两组治疗后比较差异有统计学意义(P<0.05)。结论参苓白术散能降低胃癌IV期患者外周血CD4+CD25+Tregs和单核细胞Foxp3 m RNA的表达,降低抑制性细胞因子IL-10、TGF-β1浓度,具有免疫调节作用。展开更多
目的观察NOD小鼠人源化后,CD4^+和CD8^+调节性T细胞(regulatory T cells,Tregs)频率和功能的变化,揭示Tregs在人源化NOD小鼠1型糖尿病中的作用及免疫学机制可能的变化。方法流式细胞术分别分析12周龄未发病的人源化NOD小鼠和NOD小鼠脾...目的观察NOD小鼠人源化后,CD4^+和CD8^+调节性T细胞(regulatory T cells,Tregs)频率和功能的变化,揭示Tregs在人源化NOD小鼠1型糖尿病中的作用及免疫学机制可能的变化。方法流式细胞术分别分析12周龄未发病的人源化NOD小鼠和NOD小鼠脾淋巴细胞和胰腺淋巴结细胞中CD8^+CD122^+T、CD8^+CD28-T、CD8^+CD25^+Foxp3^+T和CD4^+CD25^+Foxp3^+T细胞的频率,并采用3H-Td R掺入法检测脾CD4^+CD25^+T和CD8^+CD25^+T细胞的免疫抑制功能。结果人源化NOD小鼠和NOD小鼠的脾淋巴细胞和胰腺淋巴结细胞中CD4^+CD25^+Foxp3^+T细胞频率无显著性差异(P>0.05),而人源化NOD小鼠脾淋巴细胞和胰腺淋巴结细胞中CD8^+CD122^+T、CD8^+CD28-T、CD8^+CD25^+Foxp3^+T细胞等CD8^+Tregs亚群的频率较NOD小鼠都显著降低,但NOD小鼠人源化后,CD4^+CD25^+T和CD8^+CD25^+T细胞的免疫抑制功能并没有显著性差异;同时与人源化NOD小鼠相比,NOD小鼠的胰腺淋巴结细胞中CD8^+T细胞频率更低。结论人源化NOD小鼠脾脏和胰腺淋巴结中CD8^+Tregs亚群频率的降低,引起其胰腺淋巴结中CD8^+T细胞频率的升高,导致胰岛β细胞破坏更严重,可能是引起人源化NOD小鼠自发1型糖尿病较NOD小鼠明显提前且加重的因素之一。展开更多
肿瘤的发生是通过多种途径引起机体免疫系统调节紊乱导致的,因此抗自身抗原的免疫反应保护机理可以使肿瘤细胞免于被自身免疫系统识别。而FOXP3作为CD4^+CD25^+调节T细胞(regulatory T cells,Tregs)表面的特征性标志,可以通过下调免疫...肿瘤的发生是通过多种途径引起机体免疫系统调节紊乱导致的,因此抗自身抗原的免疫反应保护机理可以使肿瘤细胞免于被自身免疫系统识别。而FOXP3作为CD4^+CD25^+调节T细胞(regulatory T cells,Tregs)表面的特征性标志,可以通过下调免疫活化细胞因子的表达和上调Tregs相关的细胞表面分子的表达赋予CD4^+CD25^+Tregs细胞免疫抑制功能,并有效抑制机体抗肿瘤免疫反应,参与肿瘤免疫逃逸。展开更多
文摘Cellular senescence is a signal transduction process which maintained genomic stability and stopped mammalian cell growth. Furthermore, cellular senescence induces a protective response to a variety of DNA damage. However, this process is also associated with apoptosis, upregulated secretion of inflammatory cytokine, and promoted surrounding tissue damage. When cellular senescence accumulates to a certain extent, it triggers geriatric diseases, such as chronic inflammation, immune senescence-associated tumors and incontrollable infections. Cellular senescence gene SENEX, which was cloned in 2004, has been demonstrated to play a unique gatekeeper function in human endothelial cells when stress-induced pre-mature senescence and apoptosis occurr. The phenomenon that CD4+CD25+ Treg cells accumulated in the aged population has been well studied in recent years. Now Treg accumulation related to immune-pathology has attracted more interest. CD4+CD25+ Treg did not decline and age, but accumulated and suppressed immunoreaction. The enhanced Treg number and function may be associated with stress-induced premature senescence-mediated unique cellular senescence protection mechanisms, and SENEX may play a critical role in this process. In this article, we summarize the cellular senescence and SENEX gene in the accumulation and functional activity of CD4+CD25+ Treg in the elderly.
文摘目的探讨参苓白术散对胃癌IV期患者外周血CD4+CD25+Tregs、Foxp3 m RNA及血清细胞因子IL-10、TGF-β1的影响。方法将40例胃癌IV期患者随机分为观察组、对照组各20例。对照组予对症支持治疗,观察组对症支持治疗同时予参苓白术散治疗,治疗4 w后观察两组患者外周血CD4+CD25+Tregs、单核细胞Foxp3 m RNA及血清IL-10、TGF-β1浓度的变化。结果治疗后观察组患者外周血CD4+CD25+Tregs、单核细胞Foxp3 m RNA及血清IL-10、TGF-β1浓度均显著降低(P<0.05),对照组治疗后各项指标无明显变化(P>0.05),两组治疗后比较差异有统计学意义(P<0.05)。结论参苓白术散能降低胃癌IV期患者外周血CD4+CD25+Tregs和单核细胞Foxp3 m RNA的表达,降低抑制性细胞因子IL-10、TGF-β1浓度,具有免疫调节作用。
文摘目的观察NOD小鼠人源化后,CD4^+和CD8^+调节性T细胞(regulatory T cells,Tregs)频率和功能的变化,揭示Tregs在人源化NOD小鼠1型糖尿病中的作用及免疫学机制可能的变化。方法流式细胞术分别分析12周龄未发病的人源化NOD小鼠和NOD小鼠脾淋巴细胞和胰腺淋巴结细胞中CD8^+CD122^+T、CD8^+CD28-T、CD8^+CD25^+Foxp3^+T和CD4^+CD25^+Foxp3^+T细胞的频率,并采用3H-Td R掺入法检测脾CD4^+CD25^+T和CD8^+CD25^+T细胞的免疫抑制功能。结果人源化NOD小鼠和NOD小鼠的脾淋巴细胞和胰腺淋巴结细胞中CD4^+CD25^+Foxp3^+T细胞频率无显著性差异(P>0.05),而人源化NOD小鼠脾淋巴细胞和胰腺淋巴结细胞中CD8^+CD122^+T、CD8^+CD28-T、CD8^+CD25^+Foxp3^+T细胞等CD8^+Tregs亚群的频率较NOD小鼠都显著降低,但NOD小鼠人源化后,CD4^+CD25^+T和CD8^+CD25^+T细胞的免疫抑制功能并没有显著性差异;同时与人源化NOD小鼠相比,NOD小鼠的胰腺淋巴结细胞中CD8^+T细胞频率更低。结论人源化NOD小鼠脾脏和胰腺淋巴结中CD8^+Tregs亚群频率的降低,引起其胰腺淋巴结中CD8^+T细胞频率的升高,导致胰岛β细胞破坏更严重,可能是引起人源化NOD小鼠自发1型糖尿病较NOD小鼠明显提前且加重的因素之一。
文摘肿瘤的发生是通过多种途径引起机体免疫系统调节紊乱导致的,因此抗自身抗原的免疫反应保护机理可以使肿瘤细胞免于被自身免疫系统识别。而FOXP3作为CD4^+CD25^+调节T细胞(regulatory T cells,Tregs)表面的特征性标志,可以通过下调免疫活化细胞因子的表达和上调Tregs相关的细胞表面分子的表达赋予CD4^+CD25^+Tregs细胞免疫抑制功能,并有效抑制机体抗肿瘤免疫反应,参与肿瘤免疫逃逸。