目的:观察1型糖尿病(type 1 diabetes mellitus,T1DM)及成人隐匿性自身免疫性糖尿病(latent autoimmune diabetes in adults,LADA)患者外周血中调节性T细胞(regulatory T cells,Treg)、辅助性T细胞17(Helper T cell,Th17)及细胞因子白介...目的:观察1型糖尿病(type 1 diabetes mellitus,T1DM)及成人隐匿性自身免疫性糖尿病(latent autoimmune diabetes in adults,LADA)患者外周血中调节性T细胞(regulatory T cells,Treg)、辅助性T细胞17(Helper T cell,Th17)及细胞因子白介素17(interleukin-17,IL-17)的表达水平,并分析其与T1DM胰岛B细胞功能的相关性,从而探讨Th17/Treg在T1DM中的作用。方法:收集2021年12月至2022年6月就诊于蚌埠医学院第一附属医院内分泌科的1型糖尿病、成人隐匿性自身免疫性糖尿病患者及正常健康人共78例,分为T1DM组、LADA组及NC组。ELISA法检测血清IL-17,流式细胞仪检测Th17细胞及Treg细胞比例,比较三组之间各指标的表达差异。结果:T1DM组及LADA组的Treg细胞比例均低于NC组,且T1DM组低于LADA组(P<0.05)。T1DM组及LADA组的Th17及IL-17表达水平高于NC组(P<0.05),但T1DM组与LADA组之间差异无统计学意义(P>0.05)。Pearson相关性分析结果显示,血清IL-17、Th17与FCP及2 h-CP均呈负相关(P<0.05),Treg与FCP及2 h-CP呈正相关(P<0.05);以T1DM、LADA、NC为因变量(1=T1DM,2=LADA,3=NC)进行多分类logistic回归分析,结果显示IL-17是T1DM及LADA的危险因素(P<0.05),Th17为T1DM的危险因素(P<0.05),Treg为T1DM及LADA的保护因素(P<0.05)。结论:T1DM及LADA患者体内存在Th17/Treg比值的失衡,表现为Th17及IL-17的表达水平增加并伴有Treg的下降,这与胰岛B细胞功能损伤相关,可能促进T1DM的发生与发展。展开更多
Several experimental evidence suggests a link between brain Herpes simplex virus type-1 infection and the occurrence of Alzheimer’s disease.However,the molecular mechanisms underlying this association are not complet...Several experimental evidence suggests a link between brain Herpes simplex virus type-1 infection and the occurrence of Alzheimer’s disease.However,the molecular mechanisms underlying this association are not completely understood.Among the molecular mediators of synaptic and cognitive dysfunction occurring after Herpes simplex virus type-1 infection and reactivation in the brain neuroinflammatory cytokines seem to occupy a central role.Here,we specifically reviewed literature reports dealing with the impact of neuroinflammation on synaptic dysfunction observed after recurrent Herpes simplex virus type-1 reactivation in the brain,highlighting the role of interleukins and,in particular,interleukin 1βas a possible target against Herpes simplex virus type-1-induced neuronal dysfunctions.展开更多
BACKGROUND IL-22 plays a pivotal role in the processes of inflammation and tissue healing.,but its role in cholangiocarcinoma(CCA)remains unclear.our study explored the IL-22/IL-22R1 pathway and its impact on CCA prog...BACKGROUND IL-22 plays a pivotal role in the processes of inflammation and tissue healing.,but its role in cholangiocarcinoma(CCA)remains unclear.our study explored the IL-22/IL-22R1 pathway and its impact on CCA progression through the ERK1/2 signaling cascade.AIM To determine the mechanism of the IL-22/IL-22R1 pathway in CCA and provide new directions for its clinical treatment.METHODS IL-22R1 expression was assessed in human and rat CCA tissues utilizing immunohistochemical techniques,Western blot analysis,and quantitative reverse transcription PCR.The impact of IL-22 on CCA cells was assessed in vitro via tests for proliferation,migration,invasion,and apoptosis assays.The rat models of thioacetamide-induced CCA and subcutaneous xenografts in nude mice were used to assess the in vivo effects.ERK1/2 inhibitors were applied to elucidate the mechanistic role of the pathway.RESULTS IL-22R1 was overexpressed in CCA cell lines and tissues.IL-22 treatment increased the phosphorylation of ERK1/2,promoting tumor cell proliferation,migration,invasion,and resistance to apoptosis.ERK1/2 inhibition considerably reversed these effects both in vitro and in vivo.CONCLUSION The IL-22/IL-22R1 axis promotes CCA progression by activating ERK1/2 signaling.Targeting this pathway with ERK1/2 inhibitors offers potential therapeutic strategies for CCA.展开更多
文摘目的:观察1型糖尿病(type 1 diabetes mellitus,T1DM)及成人隐匿性自身免疫性糖尿病(latent autoimmune diabetes in adults,LADA)患者外周血中调节性T细胞(regulatory T cells,Treg)、辅助性T细胞17(Helper T cell,Th17)及细胞因子白介素17(interleukin-17,IL-17)的表达水平,并分析其与T1DM胰岛B细胞功能的相关性,从而探讨Th17/Treg在T1DM中的作用。方法:收集2021年12月至2022年6月就诊于蚌埠医学院第一附属医院内分泌科的1型糖尿病、成人隐匿性自身免疫性糖尿病患者及正常健康人共78例,分为T1DM组、LADA组及NC组。ELISA法检测血清IL-17,流式细胞仪检测Th17细胞及Treg细胞比例,比较三组之间各指标的表达差异。结果:T1DM组及LADA组的Treg细胞比例均低于NC组,且T1DM组低于LADA组(P<0.05)。T1DM组及LADA组的Th17及IL-17表达水平高于NC组(P<0.05),但T1DM组与LADA组之间差异无统计学意义(P>0.05)。Pearson相关性分析结果显示,血清IL-17、Th17与FCP及2 h-CP均呈负相关(P<0.05),Treg与FCP及2 h-CP呈正相关(P<0.05);以T1DM、LADA、NC为因变量(1=T1DM,2=LADA,3=NC)进行多分类logistic回归分析,结果显示IL-17是T1DM及LADA的危险因素(P<0.05),Th17为T1DM的危险因素(P<0.05),Treg为T1DM及LADA的保护因素(P<0.05)。结论:T1DM及LADA患者体内存在Th17/Treg比值的失衡,表现为Th17及IL-17的表达水平增加并伴有Treg的下降,这与胰岛B细胞功能损伤相关,可能促进T1DM的发生与发展。
基金supported by UniversitàCattolica(D1 intramural funds to RP)Italian Ministry of University and Research(PRIN 2022ZYLB7B,P2022YW7BP funds to CG).
文摘Several experimental evidence suggests a link between brain Herpes simplex virus type-1 infection and the occurrence of Alzheimer’s disease.However,the molecular mechanisms underlying this association are not completely understood.Among the molecular mediators of synaptic and cognitive dysfunction occurring after Herpes simplex virus type-1 infection and reactivation in the brain neuroinflammatory cytokines seem to occupy a central role.Here,we specifically reviewed literature reports dealing with the impact of neuroinflammation on synaptic dysfunction observed after recurrent Herpes simplex virus type-1 reactivation in the brain,highlighting the role of interleukins and,in particular,interleukin 1βas a possible target against Herpes simplex virus type-1-induced neuronal dysfunctions.
基金National Natural Science Foundation of China,No.82372194.
文摘BACKGROUND IL-22 plays a pivotal role in the processes of inflammation and tissue healing.,but its role in cholangiocarcinoma(CCA)remains unclear.our study explored the IL-22/IL-22R1 pathway and its impact on CCA progression through the ERK1/2 signaling cascade.AIM To determine the mechanism of the IL-22/IL-22R1 pathway in CCA and provide new directions for its clinical treatment.METHODS IL-22R1 expression was assessed in human and rat CCA tissues utilizing immunohistochemical techniques,Western blot analysis,and quantitative reverse transcription PCR.The impact of IL-22 on CCA cells was assessed in vitro via tests for proliferation,migration,invasion,and apoptosis assays.The rat models of thioacetamide-induced CCA and subcutaneous xenografts in nude mice were used to assess the in vivo effects.ERK1/2 inhibitors were applied to elucidate the mechanistic role of the pathway.RESULTS IL-22R1 was overexpressed in CCA cell lines and tissues.IL-22 treatment increased the phosphorylation of ERK1/2,promoting tumor cell proliferation,migration,invasion,and resistance to apoptosis.ERK1/2 inhibition considerably reversed these effects both in vitro and in vivo.CONCLUSION The IL-22/IL-22R1 axis promotes CCA progression by activating ERK1/2 signaling.Targeting this pathway with ERK1/2 inhibitors offers potential therapeutic strategies for CCA.
