目的探讨抗逆转录病毒治疗(antiretroviral treatment,ART)对HIV-1感染者(people living with HIV-1,PLWH)CD3^(+)T细胞PD-1和CD160表达及其活化凋亡水平的影响。方法收集66例慢性HIV-1感染患者,根据是否接受ART治疗,将PLWH分为non-ART...目的探讨抗逆转录病毒治疗(antiretroviral treatment,ART)对HIV-1感染者(people living with HIV-1,PLWH)CD3^(+)T细胞PD-1和CD160表达及其活化凋亡水平的影响。方法收集66例慢性HIV-1感染患者,根据是否接受ART治疗,将PLWH分为non-ART组(39例)和ART组(27例),并设置HIV-1阴性对照组(30例)。采用流式细胞术检测3组外周血CD4计数及CD3^(+)T细胞中PD-1、CD160、CD95、CD38和HLA-DR的表达,并分析3组间不同指标的差异性。结果non-ART组CD3^(+)T细胞百分比和PD-1^(+)T细胞百分比与ART组相比差异无统计学意义(P=0.8141,P>0.9999),而其CD160^(+)CD3^(+)T细胞百分比显著高于ART组(P=0.0162)。共表达分析显示,non-ART组PD-1^(+)CD160^(+)CD3^(+)T细胞百分比显著高于ART组(P=0.0121),而在单阳的CD3^(+)T性细胞(CD160^(+)PD-1^(-)和PD-1^(+)CD160-)细胞群,ART组和non-ART组差异均无统计学意义(P=0.3382,P>0.9999)。在PD-1^(+)CD160^(+)CD3^(+)T细胞CD38方面,non-ART组显著高于ART组和HIV-1阴性对照组(P=0.0005,P=0.0015),HIV-1阴性对照组和ART组差异无统计学意义(P>0.9999)。结论ART对PLWH中PD-1^(+)CD160^(+)CD3^(+)T细胞百分比及其CD38的表达具有调节作用。展开更多
The regenerative capacities of organs in adult mammals vary significantly.Unlike the liver,which possesses remarkable regenerative potential,the repair of cardiac injuries has long posed a critical medical challenge.R...The regenerative capacities of organs in adult mammals vary significantly.Unlike the liver,which possesses remarkable regenerative potential,the repair of cardiac injuries has long posed a critical medical challenge.Recent studies have highlighted the pivotal role of the immune microenvironment in repairing damage in these tissues,but the key cell types and their mechanisms of action remain incompletely understood.In this study,we established a model of concurrent physical trauma to the hearts and livers of adult mice,revealing that these two injured tissues drive distinct immune microenvironments.The liver primarily accumulates lymphocytes,whereas the heart recruits macrophages and neutrophils.Notably,CD160^(+)CD8^(+)intraepithelial lymphocytes in the liver were found to suppress fibrosis postliver injury and mitigate cardiac fibrosis when delivered via hydrogel patches.Conversely,in response to heart trauma,recruited inflammatory macrophages not only express proinflammatory cytokines but also coexpress CCRL2.While CCRL2 did not directly alter the intensity of the inflammatory response,it facilitated fibroblast proliferation and migration through its interaction with Na^(+)/K^(+)-ATPase on fibroblasts.These findings elucidated the contrasting immune microenvironments between the heart and liver following injury and provided novel insights and strategies for diagnosing and treating cardiac diseases.展开更多
文摘目的探讨抗逆转录病毒治疗(antiretroviral treatment,ART)对HIV-1感染者(people living with HIV-1,PLWH)CD3^(+)T细胞PD-1和CD160表达及其活化凋亡水平的影响。方法收集66例慢性HIV-1感染患者,根据是否接受ART治疗,将PLWH分为non-ART组(39例)和ART组(27例),并设置HIV-1阴性对照组(30例)。采用流式细胞术检测3组外周血CD4计数及CD3^(+)T细胞中PD-1、CD160、CD95、CD38和HLA-DR的表达,并分析3组间不同指标的差异性。结果non-ART组CD3^(+)T细胞百分比和PD-1^(+)T细胞百分比与ART组相比差异无统计学意义(P=0.8141,P>0.9999),而其CD160^(+)CD3^(+)T细胞百分比显著高于ART组(P=0.0162)。共表达分析显示,non-ART组PD-1^(+)CD160^(+)CD3^(+)T细胞百分比显著高于ART组(P=0.0121),而在单阳的CD3^(+)T性细胞(CD160^(+)PD-1^(-)和PD-1^(+)CD160-)细胞群,ART组和non-ART组差异均无统计学意义(P=0.3382,P>0.9999)。在PD-1^(+)CD160^(+)CD3^(+)T细胞CD38方面,non-ART组显著高于ART组和HIV-1阴性对照组(P=0.0005,P=0.0015),HIV-1阴性对照组和ART组差异无统计学意义(P>0.9999)。结论ART对PLWH中PD-1^(+)CD160^(+)CD3^(+)T细胞百分比及其CD38的表达具有调节作用。
基金supported by the National Key Research and Development Program of China(2025YFA1309100)the distinguished Young Scientist Fund of NSFC(82125016)+6 种基金the National Natural Science Foundation of China Key Program(82230061)supported by the National Natural Science Foundation of China,Special Program(82341216)the Zhejiang Provincial Natural Science Foundation of China(LHDMD22H100002)supported by the National Key Research and Development Program of China(2021YFA1101803 and 2021ZD0203304)supported by the Jiangsu Science and Technology Project(Social Development)(BE2019669)the National Natural Science Foundation of China(82071046,82100540)supported by the 111 Program(D20036).
文摘The regenerative capacities of organs in adult mammals vary significantly.Unlike the liver,which possesses remarkable regenerative potential,the repair of cardiac injuries has long posed a critical medical challenge.Recent studies have highlighted the pivotal role of the immune microenvironment in repairing damage in these tissues,but the key cell types and their mechanisms of action remain incompletely understood.In this study,we established a model of concurrent physical trauma to the hearts and livers of adult mice,revealing that these two injured tissues drive distinct immune microenvironments.The liver primarily accumulates lymphocytes,whereas the heart recruits macrophages and neutrophils.Notably,CD160^(+)CD8^(+)intraepithelial lymphocytes in the liver were found to suppress fibrosis postliver injury and mitigate cardiac fibrosis when delivered via hydrogel patches.Conversely,in response to heart trauma,recruited inflammatory macrophages not only express proinflammatory cytokines but also coexpress CCRL2.While CCRL2 did not directly alter the intensity of the inflammatory response,it facilitated fibroblast proliferation and migration through its interaction with Na^(+)/K^(+)-ATPase on fibroblasts.These findings elucidated the contrasting immune microenvironments between the heart and liver following injury and provided novel insights and strategies for diagnosing and treating cardiac diseases.
