目的:探究chemerin对银屑病患者外周血辅助性T淋巴细胞9(helper T cells 9,Th9)/调节性T淋巴细胞(regulatory T cells,Treg)免疫平衡的调节作用及其潜在的机制。方法:选取25例银屑病患者和20例健康志愿者,采用磁珠分离法分离出受试者外...目的:探究chemerin对银屑病患者外周血辅助性T淋巴细胞9(helper T cells 9,Th9)/调节性T淋巴细胞(regulatory T cells,Treg)免疫平衡的调节作用及其潜在的机制。方法:选取25例银屑病患者和20例健康志愿者,采用磁珠分离法分离出受试者外周血中CD4+T细胞,行实时RT-PCR和ELISA检测细胞中chemerin和其受体chemR23的表达;用不同浓度的chemerin(50,100,150,200 ng/mL)分别处理从健康志愿者外周血分离得到的CD4+T细胞,行MT T比色法检测细胞活力以筛选最适浓度;采用ELISA检测炎性细胞因子水平;行流式细胞术检测Th9和Treg细胞数。结果:与对照相比,银屑病患者外周血中chemerin和chemR23的表达均显著增加,T h 9/Treg比例明显上升(均P<0.05);选取最适浓度150 ng/mL的chemerin处理CD4+T细胞后,细胞中白细胞介素(IL)-6,IL-9和IL-17的水平均显著增加,Th9/Treg比例明显上升(均P<0.05),而chemR23沉默可反转chemerin对CD4+T细胞的上述作用(均P<0.05)。结论:Chemerin通过chemR23调节银屑病患者外周血CD4+T淋巴细胞中的T h 9/Treg细胞免疫平衡。展开更多
Physical exe rcise effectively alleviates chronic pain associated with complex regional pain syndrome type-Ⅰ.However,the mechanism of exe rcise-induced analgesia has not been clarified.Recent studies have shown that ...Physical exe rcise effectively alleviates chronic pain associated with complex regional pain syndrome type-Ⅰ.However,the mechanism of exe rcise-induced analgesia has not been clarified.Recent studies have shown that the specialized pro-resolving lipid mediator resolvin E1 promotes relief of pathologic pain by binding to chemerin receptor 23 in the nervous system.However,whether the resolvin E1-chemerin receptor 23 axis is involved in exercise-induced analgesia in complex regional pain syndrome type-Ⅰ has not been demonstrated.In the present study,a mouse model of chronic post-ischemia pain was established to mimic complex regional pain syndrome type-Ⅰ and subjected to an intervention involving swimming at different intensities.Chronic pain was reduced only in mice that engaged in high-intensity swimming.The resolvin E1-chemerin receptor 23 axis was clearly downregulated in the spinal cord of mice with chronic pain,while high-intensity swimming restored expression of resolvin E1 and chemerin receptor 23.Finally,shRNA-mediated silencing of chemerin receptor 23in the spinal cord reve rsed the analgesic effect of high-intensity swimming exercise on chronic post-ischemic pain and the anti-inflammato ry pola rization of microglia in the dorsal horn of the spinal cord.These findings suggest that high-intensity swimming can decrease chronic pain via the endogenous resolvin E1-chemerin receptor 23 axis in the spinal cord.展开更多
文摘目的:探究chemerin对银屑病患者外周血辅助性T淋巴细胞9(helper T cells 9,Th9)/调节性T淋巴细胞(regulatory T cells,Treg)免疫平衡的调节作用及其潜在的机制。方法:选取25例银屑病患者和20例健康志愿者,采用磁珠分离法分离出受试者外周血中CD4+T细胞,行实时RT-PCR和ELISA检测细胞中chemerin和其受体chemR23的表达;用不同浓度的chemerin(50,100,150,200 ng/mL)分别处理从健康志愿者外周血分离得到的CD4+T细胞,行MT T比色法检测细胞活力以筛选最适浓度;采用ELISA检测炎性细胞因子水平;行流式细胞术检测Th9和Treg细胞数。结果:与对照相比,银屑病患者外周血中chemerin和chemR23的表达均显著增加,T h 9/Treg比例明显上升(均P<0.05);选取最适浓度150 ng/mL的chemerin处理CD4+T细胞后,细胞中白细胞介素(IL)-6,IL-9和IL-17的水平均显著增加,Th9/Treg比例明显上升(均P<0.05),而chemR23沉默可反转chemerin对CD4+T细胞的上述作用(均P<0.05)。结论:Chemerin通过chemR23调节银屑病患者外周血CD4+T淋巴细胞中的T h 9/Treg细胞免疫平衡。
基金National Key R&D Program of China,Nos.2019YFA0110300 (to LZ),2021YFA1201400 (to LZ)Natural Science Foundation of Shanghai,No.21ZR1468600 (to LZ)Open Fund of the Key Laboratory of Cellular Physiology (Shanxi Medical University),Ministry of Education,No.KLMEC/SXMU-201910 (to XJ)。
文摘Physical exe rcise effectively alleviates chronic pain associated with complex regional pain syndrome type-Ⅰ.However,the mechanism of exe rcise-induced analgesia has not been clarified.Recent studies have shown that the specialized pro-resolving lipid mediator resolvin E1 promotes relief of pathologic pain by binding to chemerin receptor 23 in the nervous system.However,whether the resolvin E1-chemerin receptor 23 axis is involved in exercise-induced analgesia in complex regional pain syndrome type-Ⅰ has not been demonstrated.In the present study,a mouse model of chronic post-ischemia pain was established to mimic complex regional pain syndrome type-Ⅰ and subjected to an intervention involving swimming at different intensities.Chronic pain was reduced only in mice that engaged in high-intensity swimming.The resolvin E1-chemerin receptor 23 axis was clearly downregulated in the spinal cord of mice with chronic pain,while high-intensity swimming restored expression of resolvin E1 and chemerin receptor 23.Finally,shRNA-mediated silencing of chemerin receptor 23in the spinal cord reve rsed the analgesic effect of high-intensity swimming exercise on chronic post-ischemic pain and the anti-inflammato ry pola rization of microglia in the dorsal horn of the spinal cord.These findings suggest that high-intensity swimming can decrease chronic pain via the endogenous resolvin E1-chemerin receptor 23 axis in the spinal cord.
