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CD68^+、CD163^+巨噬细胞对食管癌浸润及预后的影响 被引量:9
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作者 张志斌 朱艳 席俊峰 《现代中西医结合杂志》 CAS 2015年第6期590-592,共3页
目的探讨CD68+、CD163+巨噬细胞对食管癌浸润及预后的影响。方法收集手术切除的食管癌组织标本84例、食管癌旁组织标本49例,采用免疫组化法检测组织标本中CD68+、CD163+巨噬细胞浸润密度,并对患者预后进行分析。结果食管癌组织中CD68+、... 目的探讨CD68+、CD163+巨噬细胞对食管癌浸润及预后的影响。方法收集手术切除的食管癌组织标本84例、食管癌旁组织标本49例,采用免疫组化法检测组织标本中CD68+、CD163+巨噬细胞浸润密度,并对患者预后进行分析。结果食管癌组织中CD68+、CD163+巨噬细胞浸润密度每视野(35.69±14.50)个和(29.78±12.36)个,中位数分别为32.8个和27.1个;癌旁正常组织中CD68+、CD163+巨噬细胞浸润密度每视野(4.26±2.30)个和(2.33±1.71)个,中位数分别为3.4个和2.2个。食管癌组织中CD68+、CD163+巨噬细胞浸润密度明显高于癌旁正常组织(P均<0.05)。TNMⅢ期者、有淋巴结转移者、低分化程度者CD68+、CD163+巨噬细胞浸润密度明显高于TNMⅠ~Ⅱ期者、无淋巴结转移者、高中分化程度者(P均<0.05);患者术后1年、3年、5年生存率分别为83%,67%,46%,中位生存时间为44.21个月。Spearman相关分析显示,CD68+、CD163+巨噬细胞浸润密度与患者生存时间呈现负相关性(P<0.05);多因素Cox回归分析TNM分期、淋巴结转移、分化程度、CD163+巨噬细胞浸润密度是影响患者预后的独立危险因素(P均<0.05)。结论食管癌患者局部病灶组织中CD68+、CD163+巨噬细胞浸润密度明显增高,CD163+巨噬细胞浸润密度增高是影响患者预后的独立因素。 展开更多
关键词 食管癌 ^cd68^+巨噬细胞 ^cd163^+巨噬细胞 浸润 预后
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人外周血CD68^+单核细胞体外的分选及诱导分化为破骨细胞 被引量:8
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作者 曾润铭 金大地 张忠民 《第一军医大学学报》 CSCD 北大核心 2004年第5期585-588,共4页
目的建立高纯度人活性破骨细胞方法,用于对破骨细胞生物化学和分子生物学的研究。方法用免疫磁珠法在人类外周血单核细胞中分选出CD68+细胞,用流式细胞仪分析分选效能,体外在10-8 mol/L地塞米松及25 μg/L巨噬细胞集落刺激因子的培养条... 目的建立高纯度人活性破骨细胞方法,用于对破骨细胞生物化学和分子生物学的研究。方法用免疫磁珠法在人类外周血单核细胞中分选出CD68+细胞,用流式细胞仪分析分选效能,体外在10-8 mol/L地塞米松及25 μg/L巨噬细胞集落刺激因子的培养条件下用16 μg/L可溶性核因子κB受体活化子配体诱导(s-RANKL)分化,用降钙素受体抗体免疫组化染色及抗酒石酸磷酸酶染色鉴定,扫描电镜观察骨片贴壁细胞及骨吸收陷窝。结果分选获得CD68+单核细胞纯度为(93.06±0.61)%(n=4),经核因子κB受体活化子配体诱导后降钙素受体抗体免疫组化染色阳性,抗酒石酸磷酸酶染色,扫描电镜观察有骨吸收陷窝形成。结论人外周血单核细胞中CD68+细胞是破骨前体细胞,在RANKL在诱导下分化为成熟破骨细胞。 展开更多
关键词 外周血 ^cd68^ 单核细胞 分选 诱导分化 破骨细胞 免疫磁珠
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CD68^+巨噬细胞表达与肺腺癌侵袭性及临床病理分期相关性分析 被引量:2
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作者 张倩倩 邹珏 沈丽华 《临床肺科杂志》 2019年第10期1859-1862,共4页
目的通过肺腺癌肿瘤实质中CD68^+巨噬细胞浸润情况的分析,及肿瘤实质中Ki67指数表达情况,探讨肿瘤相关巨噬细胞(TAMs)与肺腺癌临床病理分期及肿瘤侵袭能力相关性。方法选取南京市胸科医院2017年间130例肺腺癌组织切片,应用免疫组织化学... 目的通过肺腺癌肿瘤实质中CD68^+巨噬细胞浸润情况的分析,及肿瘤实质中Ki67指数表达情况,探讨肿瘤相关巨噬细胞(TAMs)与肺腺癌临床病理分期及肿瘤侵袭能力相关性。方法选取南京市胸科医院2017年间130例肺腺癌组织切片,应用免疫组织化学技术观察并计数CD68^+巨噬细胞在肺腺癌肿瘤实质及间质浸润情况及Ki67指数表达情况分析其相关性。结果(1)肺腺癌肿瘤实质内TAMs表达低于肿瘤癌旁间质内TAMs表达(P<0.05)。(2)肺腺癌肿瘤实质及间质内TAMs表达与Ki67表达有相关性(P=0.0416)。(3)Ⅲ~Ⅳ期NSCLC肿瘤实质组织中CD68^+阳性TAMs表达显著高于Ⅰ~Ⅱ期,差异有统计学意义(P<0.05)。结论结果显示CD68+巨噬细胞浸润情况与肿瘤TNM分期、及Ki67表达有一定相关性。肿瘤相关巨噬细胞(TAMs)浸润肿瘤实质及间质导致肺内炎症微环境,与肿瘤侵袭能力正相关。 展开更多
关键词 肿瘤相关巨噬细胞(TAMs) ^cd68^+巨噬细胞 KI67 腺癌 浸润
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肝癌组织中CD68^+肿瘤相关巨噬细胞数量与Ki-67蛋白表达及原发性肝癌预后的关系 被引量:7
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作者 陈利君 陈静琦 曾波航 《肿瘤防治研究》 CAS CSCD 北大核心 2016年第9期774-778,共5页
目的探讨原发性肝癌(HCC)患者肝癌组织中CD68+肿瘤相关巨噬细胞(CD68+TAM)的数量与增殖指标Ki-67及肝癌预后的关系,寻找评估肝癌预后更可靠的指标。方法应用免疫组织化学SABC法检测73例HCC组织中CD68^+TAM的分布情况及增殖指标Ki-67蛋... 目的探讨原发性肝癌(HCC)患者肝癌组织中CD68+肿瘤相关巨噬细胞(CD68+TAM)的数量与增殖指标Ki-67及肝癌预后的关系,寻找评估肝癌预后更可靠的指标。方法应用免疫组织化学SABC法检测73例HCC组织中CD68^+TAM的分布情况及增殖指标Ki-67蛋白表达,运用化学发光测定法检测血清AFP水平。结果 CD68^+TAM高密度组Ki-67阳性率明显高于低密度组(P=0.0191)。CD68^+TAM数量与HCC患者的年龄、性别无关(P>0.05),而与HCC病理分级有关(P=2.83E-04)。血清AFP水平与HCC患者的年龄、性别、病理分级无关(P>0.05)。CD68^+TAM高密度组的总生存时间显著短于低密度组(P=0.0004)。而AFP高水平组与低水平组比较,总生存时间、Ki-67阳性率差异均无统计学意义(P>0.05)。结论 HCC患者肝癌组织中CD68^+TAM数量与肝癌增殖活性密切相关,是HCC预后的独立危险因素。与AFP相比,CD68+TAM有望成为评估肝癌预后更可靠的指标。 展开更多
关键词 肝癌 ^cd68^+肿瘤相关巨噬细胞 Ki-67 AFP 预后
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CD45RO^+T细胞和CD68^+细胞在外阴上皮内非瘤样病变和外阴癌中的侵润 被引量:8
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作者 田大彤 武昕 《中国免疫学杂志》 CAS CSCD 北大核心 2008年第12期1094-1099,共6页
目的:探讨CD45RO+T细胞和CD68+细胞在外阴上皮内非瘤样病变和外阴癌发生、发展过程中的侵润及作用。方法:免疫组化S-P法分别检测CD45RO+T细胞、CD68+细胞在各20例外阴鳞状上皮细胞增生、外阴硬化性苔藓、外阴鳞状上皮癌病变中的侵润,取1... 目的:探讨CD45RO+T细胞和CD68+细胞在外阴上皮内非瘤样病变和外阴癌发生、发展过程中的侵润及作用。方法:免疫组化S-P法分别检测CD45RO+T细胞、CD68+细胞在各20例外阴鳞状上皮细胞增生、外阴硬化性苔藓、外阴鳞状上皮癌病变中的侵润,取10例外阴正常皮肤作对照。结果:CD45RO+T细胞和CD68+细胞在外阴正常皮肤中侵润水平极低,明显低于外阴鳞状上皮细胞增生、外阴硬化性苔藓和外阴鳞状细胞癌病变(P<0.05)。它们在外阴硬化性苔藓晚期病变中侵润明显高于早期病变(P<0.05);在中高分化外阴鳞状细胞癌组织中侵润明显高于低分化外阴鳞状细胞癌组织(P<0.05)。CD45RO+T细胞在中高分化外阴鳞状细胞癌组织中侵润最高,其次是晚期硬化性苔藓(P<0.05);CD68+细胞在中高分化外阴鳞状细胞癌和晚期硬化性苔藓病变中侵润最高,但二者之间没有统计学差异(P>0.05);它们均明显高于外阴鳞状细胞增生、低分化外阴鳞状细胞癌和早期硬化性苔藓(P<0.05),而在后三者之间侵润没有明显差异(P>0.05)。CD68+细胞和CD45RO+T细胞在外阴不同病变中侵润具有正相关性,相关系数为0.742(P<0.001),而且CD68+细胞多出现在CD45RO+T细胞的周围,且多在病变浅层。结论:CD45RO+T细胞和CD68+细胞参与皮肤的免疫反应,它们相互协同作用,在外阴上皮内非瘤样病变和外阴癌发生发展过程中发挥免疫调节作用。 展开更多
关键词 外阴上皮内非瘤样病变 外阴鳞状上皮癌 ^cd45RO^+T细胞 ^cd68^+细胞
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肿瘤相关巨噬细胞及CD8^(+)/CD68^(+)细胞比值是影响肺腺癌患者预后的独立危险因素
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作者 张洪玉 何娴 +4 位作者 沈琼 刘颖婷 陈陆俊 郑晓 王智刚 《中国肿瘤生物治疗杂志》 CAS CSCD 北大核心 2022年第12期1108-1114,共7页
目的:探讨CD68^(+)肿瘤相关巨噬细胞(TAM)、CD8^(+)T细胞、Foxp3^(+)Treg细胞等在肺腺癌(LUAD)组织中浸润分布及其与患者预后的关系。方法:收集2004年9月至2009年4月间在苏州大学附属第三医院手术切除的93例LUAD组织及78例癌旁组织,采... 目的:探讨CD68^(+)肿瘤相关巨噬细胞(TAM)、CD8^(+)T细胞、Foxp3^(+)Treg细胞等在肺腺癌(LUAD)组织中浸润分布及其与患者预后的关系。方法:收集2004年9月至2009年4月间在苏州大学附属第三医院手术切除的93例LUAD组织及78例癌旁组织,采用组织芯片(TMA)及多重免疫荧光(mIF)技术检测其中的免疫细胞浸润与分布,Wilcoxon秩和检验比较癌与癌旁组织、癌巢与间质中浸润水平的差异,χ^(2)检验分析其浸润水平及CD8^(+)/CD68^(+)细胞比值与临床病理特征的关系,Kaplan-Meier法和COX模型分析影响患者OS的潜在危险因素。结果:与癌旁组织比较,癌组织中CD68^(+)TAM、CD8^(+)T细胞、Foxp3^(+)Treg细胞浸润水平均显著增加(均P<0.01),间质CD68^(+)TAM、CD8^(+)T细胞的浸润水平均显著高于癌巢(均P<0.01)。总CD68^(+)TAM、癌巢及间质CD68^(+)TAM浸润水平与淋巴结转移呈正向关联(均P<0.05),癌巢CD68^(+)TAM浸润水平与T分期呈正向关联(P<0.05),间质CD68^(+)TAM浸润水平与病理分级呈正向关联(P<0.05);癌组织中CD8^(+)/CD68^(+)细胞比值与病理分级、淋巴结转移均呈负向关联(均P<0.05)。Kaplan-Meier生存分析显示,LUAD组织中总CD68^(+)TAM、癌巢及间质CD68^(+)TAM高浸润患者OS均短于低浸润患者(P<0.05或P<0.01)、癌组织中CD8^(+)/CD68^(+)细胞比值高患者OS显著长于低比值患者(P<0.05)。多因素COX模型分析示,LUAD患者年龄、TNM分期及癌组织中CD8^(+)/CD68^(+)细胞比值是影响患者预后的独立风险因素(P<0.05或P<0.01)。结论:高度浸润的CD68^(+)TAM与LUAD的进展、侵袭、转移和不良预后显著关联,而高CD8^(+)/CD68^(+)细胞比值是影响LUAD患者OS的独立保护因素。 展开更多
关键词 肺腺癌 肿瘤相关巨噬细胞 T细胞 TREG细胞 ^cd8^(+)/cd68^(+) 预后 多重免疫荧光技术
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CypA/CD147及MMP-2在人慢性牙周炎牙龈组织中CD68^(+)细胞上表达的研究 被引量:3
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作者 余施雷 李娟 +1 位作者 杨婷 黄世光 《中国病理生理杂志》 CAS CSCD 北大核心 2022年第11期2055-2062,共8页
目的:观察亲环素A(CypA)、CD147及基质金属蛋白酶2(MMP-2)在人慢性牙周炎患者牙龈组织中CD68^(+)细胞(单核细胞/巨噬细胞)的表达情况,探讨CD68^(+)细胞中CypA、CD147及MMP-2在不同病变程度牙周炎牙龈组织中的表达及作用机制。方法:将60... 目的:观察亲环素A(CypA)、CD147及基质金属蛋白酶2(MMP-2)在人慢性牙周炎患者牙龈组织中CD68^(+)细胞(单核细胞/巨噬细胞)的表达情况,探讨CD68^(+)细胞中CypA、CD147及MMP-2在不同病变程度牙周炎牙龈组织中的表达及作用机制。方法:将60例受试者分为4组,每组15例,分别为:健康组及慢性牙周炎(轻、中、重)组。免疫荧光双染色(DIF)后荧光显微镜下分别观察牙龈组织中CD68-CypA、CD68-CD147及CD68-MMP-2双阳性细胞表达情况并计算单位面积双阳性细胞密度。结果:(1)各组牙龈组织中CD68-CypA、CD68-CD147及CD68-MMP-2双阳性细胞密度差异显著(P<0.01);(2)各组牙龈组织中CD68-CypA双阳性细胞(r=0.959,P=0.000)、CD68-CD147双阳性细胞(r=0.948,P=0.000)及CD68-MMP-2双阳性细胞密度(r=0.945,P=0.000)与牙周炎的严重程度呈正相关;(3)各组牙龈组织中CD68-CypA与CD68-MMP-2双阳性表达正向相关(r=0.933,P=0.000);CD68-CD147与CD68-MMP-2双阳性表达水平正相关(r=0.954,P=0.000)。结论:牙龈组织中CD68-CypA、CD68-CD147及CD68-MMP2双阳性细胞密度随牙周病程加重而增多,且CD68-CypA和CD68-CD147双阳性细胞的密度与CD68-MMP-2双阳性细胞密度呈正相关。 展开更多
关键词 慢性牙周炎 ^cd68^(+)细胞 亲环素A cd147 基质金属蛋白酶2
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乳腺癌T淋巴细胞及CD68^(+)肿瘤相关巨噬细胞浸润的临床病理观察
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作者 徐钢 《中国现代药物应用》 2022年第18期80-82,共3页
目的分析乳腺癌T淋巴细胞、CD68^(+)肿瘤相关巨噬细胞(TAM)浸润的临床病理意义。方法60例初治乳腺癌患者,以免疫组织化学法检测患者术后组织标本T淋巴细胞、CD68^(+)TAM表达情况及Ki-67增殖指数表达情况,分析光学显微镜下T淋巴细胞数、C... 目的分析乳腺癌T淋巴细胞、CD68^(+)肿瘤相关巨噬细胞(TAM)浸润的临床病理意义。方法60例初治乳腺癌患者,以免疫组织化学法检测患者术后组织标本T淋巴细胞、CD68^(+)TAM表达情况及Ki-67增殖指数表达情况,分析光学显微镜下T淋巴细胞数、CD68^(+)TAM数。比较不同Ki-67增殖指数患者的T淋巴细胞、CD68^(+)TAM表达情况,分析T淋巴细胞数和CD68^(+)TAM数与临床特征的关系。结果Ki-67增值指数≥14%、≥20%、≥30%患者的T淋巴细胞低表达率比较差异无统计学意义(P>0.05);Ki-67增殖指数≥50%患者的T淋巴细胞低表达率85.71%高于Ki-67增值指数≥14%患者,差异具有统计学意义(P<0.05);Ki-67增殖指数≥14%、≥20%、≥30%、≥50%患者的CD68^(+)TAM低表达率对比差异无统计学意义(P>0.05)。不同年龄、组织学分级、HER2(-或+)患者的T淋巴细胞数比较差异均无统计学意义(P>0.05);肿块直径≤3 cm患者的T淋巴细胞数(175.05±20.50)个/HPF高于>3 cm患者的(148.50±18.50)个/HPF,淋巴转移阴性患者的T淋巴细胞数(174.50±20.50)个/HPF高于阳性患者的(147.02±22.20)个/HPF,ER+患者的T淋巴细胞数(182.20±10.30)个/HPF高于ER-患者的(133.30±10.50)个/HPF,PR+患者的T淋巴细胞数(179.50±14.50)个/HPF高于PR-患者的(165.40±24.50)个/HPF,差异具有统计学意义(P<0.05)。不同肿块直径、ER(-或+)、PR(-或+)患者的CD68^(+)TAM数比较差异均无统计学意义(P>0.05);年龄≤51岁患者的CD68^(+)TAM数(90.95±9.50)个/HPF高于>51岁患者的(83.30±8.08)个/HPF,组织学分级Ⅲ级患者的CD68^(+)TAM数(91.55±8.50)个/HPF高于Ⅰ~Ⅱ级患者的(85.20±8.80)个/HPF,淋巴转移阳性患者的CD68^(+)TAM数(90.99±9.02)个/HPF高于阴性患者的(84.50±9.60)个/HPF,HER2+患者的CD68^(+)TAM数(92.30±8.20)个/HPF高于HER2-患者的(84.08±8.50)个/HPF,差异具有统计学意义(P<0.05)。结论浸润CD68^(+)TAM与乳腺癌的进展关系密切,有助于临床工作的开展。 展开更多
关键词 乳腺癌 T淋巴细胞 ^cd68^(+)肿瘤相关巨噬细胞 临床病理
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Promotion of Sema4D expression by tumor-associated macrophages: Significance in gastric carcinoma 被引量:7
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作者 Han Li Jin-Shen Wang +3 位作者 Lin-Jun Mu Ke-Shu Shan Le-Ping Li Yan-Bing Zhou 《World Journal of Gastroenterology》 SCIE CAS 2018年第5期593-601,共9页
AIM To study the role of semaphorin 4 D(Sema4 D) expression promoted by tumor-associated macrophages(TAMs) in gastric carcinoma cells and its clinical significance in the invasion and metastasis of gastric carcinoma.M... AIM To study the role of semaphorin 4 D(Sema4 D) expression promoted by tumor-associated macrophages(TAMs) in gastric carcinoma cells and its clinical significance in the invasion and metastasis of gastric carcinoma.METHODS CD68 and Sema4 D expression was analyzed in gastric carcinoma and adjacent normal tissues from 290 patients using the immunohistochemical streptavidinperoxidase method, and their relationships with clinicopathological features were evaluated. Human M2 macrophages were induced in vitro and co-cultured in non-contact with gastric carcinoma SGC-7901 cells. Changes in the secretory Sema4 D level in the SGC-7901 cell supernatant were measured using an enzymelinked immunosorbent assay. The effects of TAMs on SGC-7901 cell invasion and migration were assessed with invasion and migration assays, respectively.RESULTS CD68 and Sema4 D protein expression was significantly higher in gastric carcinoma tissues than in adjacent normal tissues(71.7% vs 33.8% and 74.5% vs 42.8%, respectively; P < 0.01). CD68 and Sema4 D protein expression was significantly associated with histological differentiation, TNM stage, and lymph node metastasis(P < 0.05), and their expression levels were positively correlated with one another(r = 0.467, P < 0.01). In the in vitro experiment, secretory Sema4 D protein expression was significantly increased in the supernatant of SGC-7901 cells co-cultured with TAMs compared with the blank control(1224.13 ± 29.43 vs 637.15 ± 33.84, P < 0.01). Cell invasion and metastasis were enhanced in the Transwell invasion and migration assays(P < 0.01).CONCLUSION TAMs promote the invasion and metastasis of gastric carcinoma cells possibly through upregulated secretory Sema4 D protein expression. Combined detection of TAM markers, CD68 and Sema4 D, in gastric carcinoma tissue shows potential to predict the trend of gastric carcinoma progression. 展开更多
关键词 Gastric carcinoma cd68 SEMAPHORIN 4D TUMOR-ASSOCIATED macrophages
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IGF2BP3 Enhances the Growth of Hepatocellular Carcinoma Tumors by Regulating the Properties of Macrophages and CD8^(+)T Cells in the Tumor Microenvironment
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作者 Lingyu Ma Jiayu Jiang +2 位作者 Qin Si Chong Chen Zhaojun Duan 《Journal of Clinical and Translational Hepatology》 SCIE 2023年第6期1308-1320,共13页
Background and Aims:Overexpression of IGF2BP3 is associated with the prognosis of hepatocellular carcinoma(HCC).However,its role in regulating tumor immune microenvironment(TME)is not well characterized.Here,we invest... Background and Aims:Overexpression of IGF2BP3 is associated with the prognosis of hepatocellular carcinoma(HCC).However,its role in regulating tumor immune microenvironment(TME)is not well characterized.Here,we investigated the effects of IGF2BP3 on macrophages and CD8^(+)T cells within the TME of HCC.Methods:The relationship between IGF2BP3 and immune cell infiltration was analyzed using online bioinformatics tools.Knockout of IGF2BP3 in mouse hepatoma cell line Hepa1-6 was established using CRISPR/Cas9 technology.In vitro cell coculture and subcutaneously implanted hepatoma mice model were used to explore the effects of IGF2BP3 on immune cells.Expression of CCL50l transforming growth factor beta 1(TGF-β1)was detected with quantitative real-time polymerase chain reaction,western blotting,and enzyme-linked immunosorbent assay.The binding of IGF2BP3 and its target RNA was verified by trimolecular fluorescence complementation system and RNA immunoprecipitation followed by quantitative or semiquantitative polymerase chain reaction.Results:IGF2BP3 expression was elevated in HCC and was positively correlated with macrophage infiltration.Patients with higher IGF2BP3 expression and lower macrophage infiltration had a better survival rate.We found that IGF2BP3 could bind to the mRNA of CCL5 or TGF-β1,increasing their expression,and inducing macrophage infiltration and M2 polarization while inhibiting the activation of CD8^(+)T cells.Furthermore,inhibition of IGF2BP3 combined with anti-CD47 antibody treatment significantly suppressed the growth of hepatoma in Hepa1-6 xenograft tu-mor mice.Conclusions:IGF2BP3 promoted the infiltration and M2-polarization of macrophages and suppressed CD8^(+)T activation by enhancing CCL5 and TGF-β1 expression,which facilitated the progression of Hepa1-6 xenograft tumor. 展开更多
关键词 Hepatocellular carcinoma IGF2BP3 TGF-β1 CCL5 M2 macrophage ^cd8^(+)T cell
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Crosstalk between IL-15Rα^(+)tumor-associated macrophages and breast cancer cells reduces CD8+T cell recruitment 被引量:1
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作者 Wenlong Zhang Qing Zhang +7 位作者 Nanfei Yang Qian Shi Huifang Su Tingsheng Lin Zhonglei He Wenxin Wang Hongqian Guo Pingping Shen 《Cancer Communications》 SCIE 2022年第6期536-557,共22页
Background:Interleukin-15(IL-15)is a promising immunotherapeutic agent owing to its powerful immune-activating effects.However,the clinical benefits of these treatments are limited.Crosstalk between tumor cells and im... Background:Interleukin-15(IL-15)is a promising immunotherapeutic agent owing to its powerful immune-activating effects.However,the clinical benefits of these treatments are limited.Crosstalk between tumor cells and immune cells plays an important role in immune escape and immunotherapy drug resistance.Herein,this study aimed to obtain in-depth understanding of crosstalk in the tumor microenvironment for providing potential therapeutic strategies to prevent tumor progression.Methods:T-cell killing assays and co-culture models were developed to determine the role of crosstalk between macrophages and tumor cells in breast cancer resistant to IL-15.Western blotting,histological analysis,CRISPR-Cas9 knockout,multi-parameter flow cytometry,and tumor cell-macrophage co-injection mouse models were developed to examine the mechanism by which IL-15Rα^(+)tumor-associated macrophages(TAMs)regulate breast cancer cell resistance to IL-15.Results:We found thatmacrophages contributed to the resistance of tumor cells to IL-15,and tumor cells induced macrophages to express high levels of theαsubunit of the IL-15 receptor(IL-15Rα).Further investigation showed that IL-15Rα^(+)TAMs reduced the protein levels of chemokine CX3C chemokine ligand 1(CX3CL1)in tumor cells to inhibit the recruitment of CD8^(+)T cells by releasing the IL-15/IL-15Rαcomplex(IL-15Rc).Administration of an IL-15Rc blocking peptide markedly suppressed breast tumor growth and overcame the resistance of cancer cells to anti-programmed cell death protein 1(PD-1)antibody immunotherapy.Interestingly,Granulocyte-macrophage colony-stimulating factor(GMCSF)inducedγchain(γc)expression to promote tumor cell-macrophage crosstalk,which facilitated tumor resistance to IL-15.Additionally,we observed that the non-transcriptional regulatory function of hypoxia inducible factor-1alpha(HIF-1α)was essential for IL-15Rc to regulateCX3CL1 expression in tumor cells.Conclusions:The IL-15Rc-HIF-1α-CX3CL1 signaling pathway serves as a crosstalk between macrophages and tumor cells in the tumormicroenvironment of breast cancer.Targeting this pathway may provide a potential therapeutic strategy for enhancing the efficacy of cancer immunotherapy. 展开更多
关键词 breast cancer ^cd8^(+)T-cell CROSSTALK IL-15Rα immunotherapy tumor microenvironment tumor-associated macrophages
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CD57^+自然杀伤细胞及CD68^+巨噬细胞浸润密度对食管癌患者预后的影响 被引量:2
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作者 徐斌 陈陆俊 +5 位作者 邓海峰 陆明洋 李敏 刘检 吴昌平 蒋敬庭 《中华实验外科杂志》 CAS CSCD 北大核心 2016年第4期1117-1121,共5页
目的 探讨食管癌上皮组织中CD57^+自然杀伤细胞(NK)及CD68^+巨噬细胞浸润密度与临床病理特征的相关性及对食管癌患者预后的影响.方法 应用免疫组织化学方法检测138例Ⅱ~Ⅲ期食管癌患者组织中CD57^+ NK及CD68^+巨噬细胞的浸润水平... 目的 探讨食管癌上皮组织中CD57^+自然杀伤细胞(NK)及CD68^+巨噬细胞浸润密度与临床病理特征的相关性及对食管癌患者预后的影响.方法 应用免疫组织化学方法检测138例Ⅱ~Ⅲ期食管癌患者组织中CD57^+ NK及CD68^+巨噬细胞的浸润水平,采用x2检验分析其浸润密度与临床病理特征的相关性,拟合多因素Cox模型分析上述指标对食管癌患者生存时间及预后的影响.结果 CD57^+ NK及CD68^+巨噬细胞浸润水平与人口学及临床病理特征无明显相关;在调整了性别、年龄、肿瘤大小及TNM分期的影响后,食管癌肿瘤组织中CD57^+ NK细胞浸润水平高的患者具有更低的死亡风险[风险比(HR)=0.615,95%可信区间(CI):0.405~0.933,P<0.05];CD68^+巨噬细胞浸润水平高的食管癌患者具有更高的死亡风险(HR=1.499,95%CI:1.008~2.230,P <0.05);CD57^+ NK细胞浸润水平低并且CD68^+巨噬细胞浸润水平高的食管癌患者具有更高的死亡风险(HR=2.573,95% CI:1.408 ~4.701,P<0.01);联合CD57、CD68阳性细胞浸润密度构建的Cox模型具有更好的拟合优度.结论 食管癌组织中CD57^+ NK和CD68^+巨噬细胞浸润密度均为独立预后因素,两者联合检测具有更优的预后判断能力. 展开更多
关键词 ^cd57^+自然杀伤细胞 ^cd68^+巨噬细胞 食管癌
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High baseline tumor burden-associated macrophages promote an immunosuppressive microenvironment and reduce the efficacy of immune checkpoint inhibitors through the IGFBP2-STAT3-PD-L1 pathway
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作者 Zhaowei Wen Huiying Sun +7 位作者 Zhihua Zhang Yannan Zheng Siting Zheng Jianping Bin Yulin Liao Min Shi Rui Zhou Wangjun Liao 《Cancer Communications》 SCIE 2023年第5期562-581,共20页
Background:Several clinical studies have uncovered a negative correlation between baseline tumor burden and the efficacy of immune checkpoint inhibitor(ICI)treatment.This study aimed to uncover the specific mechanisms... Background:Several clinical studies have uncovered a negative correlation between baseline tumor burden and the efficacy of immune checkpoint inhibitor(ICI)treatment.This study aimed to uncover the specific mechanisms underlying the difference in sensitivity to ICI treatment between tumors with high(HTB)and low(LTB)tumor burden.Methods:For in vivo studies,several mouse models of subcutaneous tumors were established,and transcriptome sequencing,immunohistochemistry,and flow cytometry assays were used to detect the immune status in these subcutaneous tumors.For in vitro experiments,co-culture models,cytokine antibody arrays,western blotting,flow cytometry,and enzyme-linked immunosorbent assays were used to explore the underlying molecular mechanisms Results:We found that MC38 or B16 subcutaneous tumors from the HTB group did not show any response to anti-programmed cell death protein-1(PD-1)therapy.Through flow cytometry assays,we found that the infiltration with CD8^(+)T cellswas significantly decreasedwhereasM2-like macrophageswere enriched in subcutaneous tumors of HTB groups compared with those of LTB group.These changes were not affected by the initial number of injected tumor cells or tumor age,nor could they be reversed by surgical tumor reduction.Intraperitoneal colony-stimulating factor 1 receptor(CSF-1R)inhibitor PLX3397 injection at different time points of tumor growth only had an effect when administered in the early tumor stage to maintain the“heat”of the tumor microenvironment during the process of tumor growth,thereby achieving a response to ICI treatment when the tumor grew to a large size.Mechanistically,we found that insulin-like growth factor binding protein 2(IGFBP2)expression levelswere significantly elevated in HTB tumor tissues.IGFBP2 promoted the programmed death-ligand 1(PD-L1)expression in M2-like macrophages by activating signal transducer and activator of transcription 3(STAT3),and PD-L1^(+)M2-likemacrophages exerted an immunosuppressive effect by inhibiting the proliferation and activation of CD8^(+)T cells in a PD-L1-dependent fashion.Conclusions:This study suggested that the low efficacy of ICI treatment in HTB tumors is mainly attributed to the intratumoral accumulation of PD-L1^(+)M2-like macrophages via the IGFBP2-STAT3-PD-L1 signaling pathway and their substantial inhibitory effects on T cell proliferation and activation. 展开更多
关键词 ^cd8^(+)T cell IGFBP2 immune checkpoint inhibitor macrophage PD-L1 STAT3 tumor burden tumor immune microenvironment
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小气道病变患者小气道黏膜层免疫病理的变化 被引量:3
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作者 李玉 薛玉文 +2 位作者 吴大玮 王玲 许仁和 《基础医学与临床》 CSCD 北大核心 2004年第6期642-645,共4页
探讨小气道病变患者小气道黏膜层的免疫病理学特点。 86例因肺局限性病变需行肺叶切除患者 ,分为小气道病变组 34例、COPD组 2 2例及肺功能正常组 30例。收集术后肺标本 ,应用免疫组化法检测小气道黏膜层内CD3+ 、CD8+ 、CD6 8+ 、CD4 5... 探讨小气道病变患者小气道黏膜层的免疫病理学特点。 86例因肺局限性病变需行肺叶切除患者 ,分为小气道病变组 34例、COPD组 2 2例及肺功能正常组 30例。收集术后肺标本 ,应用免疫组化法检测小气道黏膜层内CD3+ 、CD8+ 、CD6 8+ 、CD4 5RA+ 、CD4 5RO+ 、CD2 0 + 细胞 ,并与FEV1 0、V5 0、V2 5做相关性分析。小气道病变组、COPD组CD3+ 、CD8+ 、CD6 8+ 细胞数明显高于正常组 ;而小气道病变组与COPD组相比无差异 ;小气道病变组CD8+ 细胞数与V5 0呈显著负相关 ;正常组内吸烟者CD4 5R0 + 细胞数明显高于非吸烟者 ;在小气道病变组或COPD组内 ,吸烟与非吸烟者之间CD3+ 、CD8+ 、CD4 5RO+ 细胞数均无差异 ;小气道病变组内非吸烟者CD6 8+ 细胞数高于吸烟者及正常非吸烟者。T淋巴细胞尤其CD8+ 细胞及CD6 8+ 细胞在小气道病变及COPD炎性过程中有重要意义 ,吸烟可导致CD4 5RO+ 细胞在小气道黏膜集聚 ,CD6 8+ 在非吸烟因素致小气道病变中意义更大。 展开更多
关键词 小气道病变 cd68 COPD 黏膜层 正常 患者 ^cd3^+ 集聚 吸烟者 局限性
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共刺激分子在Behcet病患者结节红斑组织中的表达 被引量:4
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作者 王红 杨培增 +3 位作者 彭晓燕 周红颜 黄祥坤 刘云霞 《首都医科大学学报》 CAS 2005年第3期258-262,共5页
目的探讨Behcet病患者结节红斑中B7:CD28/CTLA-4的表达及意义。方法采用免疫组化方法对5例Behcet病活动期患者腿或臂部结节红斑中CD4、CD8、CD19、CD68、HLA-DR、B7-1、B7-2、CD28和CTLA-4分子表达的情况进行了检测,并用双重染色方法探... 目的探讨Behcet病患者结节红斑中B7:CD28/CTLA-4的表达及意义。方法采用免疫组化方法对5例Behcet病活动期患者腿或臂部结节红斑中CD4、CD8、CD19、CD68、HLA-DR、B7-1、B7-2、CD28和CTLA-4分子表达的情况进行了检测,并用双重染色方法探讨了细胞来源。结果Behcet病结节红斑中表皮约90%的细胞表达B7-1和B7-2,但无CD28和CTLA-4表达。真皮和皮下表达CD4、CD8、CD19、CD68、HLA-DR、CD1a、CD28、CTLA-4、B7-1和B7-2的细胞均显著增多。双染结果显示,100%CD4+T细胞表达CD28分子,47.9%的CD4+T细胞表达CTLA-4分子。100%CD68+细胞表达B7-1和B7-2分子。分别有74.5%和60.8%的HLA-DR+细胞表达B7-1和B7-2分子。结论CD28和CTLA-4分子主要表达于CD4+T细胞,B7-1和B7-2分子主要表达于单核巨噬细胞、抗原提呈细胞和角朊细胞。B7:CD28/CTLA-4通路可诱导巨噬细胞和T淋巴细胞的功能和活性,对Behcet病患者结节红斑的发生、炎症的持续和扩大起重要作用。 展开更多
关键词 BEHCET病 结节红斑 B7:cd28/CTLA-4 共刺激分子 患者 ^cd4^+T细胞 T细胞表达 组织 免疫组化方法 cd28分子 单核巨噬细胞 抗原提呈细胞 cd19 cd68 T淋巴细胞 HLA 分子表达 细胞来源 染色方法 cd1A 角朊细胞 cd8 表达及
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结直肠癌中肿瘤相关巨噬细胞及基因表型的分析研究 被引量:1
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作者 武艳飞 白雪峰 王智 《中国现代医生》 2019年第17期36-40,F0003,共6页
目的结直肠癌(Colorectal cancer,CRC)中肿瘤相关巨噬细胞(TAMs)CD68^+及CD163^+的检测及与基因表型的关系。方法免疫组化方法检测41例CRC肿物,癌旁5 cm(M5)、10cm(M10)。不典型增生(Atypicalhyperplasia,AH)组织CD68^+及CD163^+的表达... 目的结直肠癌(Colorectal cancer,CRC)中肿瘤相关巨噬细胞(TAMs)CD68^+及CD163^+的检测及与基因表型的关系。方法免疫组化方法检测41例CRC肿物,癌旁5 cm(M5)、10cm(M10)。不典型增生(Atypicalhyperplasia,AH)组织CD68^+及CD163^+的表达,采用病理切片扫描仪细胞计数。对41例CRC肿物进行基因检测。结果 CRC患者CD68^+及CD163^+检测肿物组织高于癌旁5cm、10cm(P<0.01);肿物与不典型组织比较差异无统计学意义(P>0.05);癌旁组织M5与M10比较差异无统计学意义(P>0.05);回归分析提示CD163^+表达与K-ras基因突变有显著性关系(P<0.05)。CD68^+及CD163^+的表达与B-raf基因突变、MSS(微卫星稳定型)、淋巴结转移、脉管癌栓、神经侵犯无相关性(P>0.05)。结论CD68^+及CD163^+在结直肠癌肿物间质中高表达,并高于癌旁组织,与AH表达无相关性。CD163^+在肿物的表达与K-ras基因突变有相关性。 展开更多
关键词 结直肠癌 ^cd68^+ ^cd163^+ 基因检测 病理切片扫描仪
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A Critical Role of Activin A in Maturation of Mouse Peritoneal Macrophages in vitro and in vivo 被引量:2
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作者 Yinan Wang Xueling Cui +5 位作者 Guixiang Tai Jingyan Ge Nan Li Fangfang Chen Fang Yu Zhonghui Liu 《Cellular & Molecular Immunology》 SCIE CAS CSCD 2009年第5期387-392,共6页
Activin A, a multifunctional factor of the transforming growth factor-beta (TGF-β) superfamily, is mainly produced by microglia and macrophages, and its anti-inflammatory and pro-inflammatory activities are both re... Activin A, a multifunctional factor of the transforming growth factor-beta (TGF-β) superfamily, is mainly produced by microglia and macrophages, and its anti-inflammatory and pro-inflammatory activities are both related to macrophage functions. However the direct effect of activin A on the rest macrophages in vivo remains unclear. In the present study, the results showed that activin A not only increased NO and IL-1β release, but also promoted phagocytic abilities of mouse peritoneal macrophages in vitro and in vivo, whereas it did not influence MHC Ⅰ and MHC Ⅱ expression. Moreover, we found that activin A significantly upregulated the expressions of CD14 and CD68, markers of mature macrophages, on the surface of macrophages in vitro and in vivo. These data suggest that activin A can induce primary macrophage maturation in vitro and in vivo, but may not trigger the acquired immune response via regulating expression of MHC molecules involved in presentation of antigen. 展开更多
关键词 activin A macrophagE MATURATION cd68 cd14
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Sodium chloride exacerbates dextran sulfate sodiuminduced colitis by tuning proinflammatory and antiinflammatory lamina propria mononuclear cells through p38/MAPK pathway in mice 被引量:1
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作者 Hong-Xia Guo Nan Ye +7 位作者 Ping Yan Min-Yue Qiu Ji Zhang Zi-Gang Shen Hai-Yang He Zhi-Qiang Tian Hong-Li Li Jin-Tao Li 《World Journal of Gastroenterology》 SCIE CAS 2018年第16期1779-1794,共16页
AIM To investigate the influence of high salt on dextran sulfate sodium(DSS)-induced colitis in mice and explore the underlying mechanisms of this effect.METHODS DSS and NaC l were used to establish the proinflammator... AIM To investigate the influence of high salt on dextran sulfate sodium(DSS)-induced colitis in mice and explore the underlying mechanisms of this effect.METHODS DSS and NaC l were used to establish the proinflammatory animal model. We evaluated the colitis severity. Flow cytometry was employed for detecting the frequencies of Th1, macrophages and Tregs in spleen, mesenteric lymph node and lamina propria. The important role of macrophages in the promotion of DSS-induced colitis by NaCl was evaluated by depleting macrophages with clodronate liposomes. Activated peritoneal macrophages and lamina propria mononuclear cells(LPMCs) were stimulated with NaCl, and proteins were detected by western blotting. Cytokines and inflammation genes were analyzed by enzyme-linked immunosorbent assay and RT-PCR, respectively.RESULTS The study findings indicate that NaC l up-regulates the frequencies of CD11b^+ macrophages and CD4^+IFN-γ^+IL-17^+ T cells in lamina propria in DSS-treated mice. CD3^+CD4^+CD25^+Foxp^3+ T cells, which can secrete high levels of IL-10 and TGF-β, increase through feedback in NaCl-and DSS-treated mice. Furthermore, clodronate liposomes pretreatment significantly alleviated DSSinduced colitis, indicating that macrophages play a vital role in NaCl proinflammatory activity. NaCl aggravates peritoneal macrophage inflammation by promoting the expressions of interleukin(IL)-1, IL-6 and mouse inducible nitric oxide synthase. Specifically, high NaCl concentrations promote p38 phosphorylation in lipopolysaccharide-and IFN-γ-activated LPMCs mediated by SGK1. CONCLUSION Proinflammatory macrophages may play an essential role in the onset and development of NaCl-promoted inflammation in DSS-induced colitis. The underlining mechanism involves up-regulation of the p38/MAPK axis. 展开更多
关键词 inflammatory BOWEL disease macrophagE NaCl ^cd4^+IFN-γ^+IL-17^+T cell p38/MAPK
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Toll样受体4基因敲除对心肌缺血的影响
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作者 王平 王睿琪 杜广胜 《农垦医学》 2019年第1期1-5,共5页
目的:研究干预Toll样受体4(Toll-Like receptor 4,TLR4)对心肌缺血小鼠脾脏中CD20^+细胞和CD68^+细胞的影响。方法:20只6周龄雄性C57BL/6野生型小鼠和20只6周龄雄性TLR4基因敲除(TLR4^-/-)小鼠分别随机设置空白对照组(NC组)、心肌缺血组... 目的:研究干预Toll样受体4(Toll-Like receptor 4,TLR4)对心肌缺血小鼠脾脏中CD20^+细胞和CD68^+细胞的影响。方法:20只6周龄雄性C57BL/6野生型小鼠和20只6周龄雄性TLR4基因敲除(TLR4^-/-)小鼠分别随机设置空白对照组(NC组)、心肌缺血组(MI组)、TLR4^-/-对照组(TLR4^-/-NC组)、TLR4^-/-心肌缺血组(TLR4^-/-MI组),每组各10只。对照组给予腹腔注射20mg/kg生理盐水(NC)7天,心肌缺血组通过给予腹腔注射20mg/kg异丙肾上腺素(isoproterenol,ISO)7天建立心肌缺血模型。造模后使用心脏超声检查小鼠心脏射血分数(ejection fraction,EF)和左室短轴缩短率(left ventricular fractional shortening,LVFS),苏木精-伊红(hematoxylin-eosin,HE)染色和天狼猩红染色观察心肌病理学变化,原位末端标记法(terminal deoxynucleotidyl transferase dUTP nick end labeling,TUNEL)检测心肌组织中凋亡水平,以及流式细胞术(Flow cytometry, FCM)检测脾脏中CD20^+细胞、CD68^+细胞含量。结果:与NC组相比,MI组心肌纤维化加重,EF和LVFS降低,脾脏组织中CD20^+细胞、CD68^+细胞含量升高(均P<0.05);与MI组相比,TLR4^-/-MI组心肌组织损伤和纤维化程度减轻,EF和LVFS升高,脾脏组织中CD20^+细胞、CD68^+细胞含量下降(均P<0.05);结论:TLR4基因敲除对于小鼠心肌缺血有保护作用,心肌细胞损伤及炎症浸润程度减轻,脾脏中CD20^+细胞、CD68^+细胞含量减少,这可能和TLR4参与调节CD20^+细胞、CD68^+细胞在心肌缺血中的免疫反应有关。 展开更多
关键词 心肌缺血 ^cd20^+细胞 ^cd68^+细胞 TOLL样受体4
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鼻息肉组织中炎性细胞的病理学意义 被引量:3
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作者 孔红 杨继红 +2 位作者 董震 杨占泉 卜国铉 《临床耳鼻咽喉科杂志》 CSCD 1999年第8期339-340,共2页
目的:研究鼻息肉组织中炎性细胞的病理意义。方法:对 10 例正常鼻粘膜和24 例鼻息肉组织行免疫组化及 M G G 染色以观察嗜酸性粒细胞、单核细胞、巨噬细胞在组织中的分布程度。结果:鼻息肉组织中嗜酸性粒细胞、 C D68 阳... 目的:研究鼻息肉组织中炎性细胞的病理意义。方法:对 10 例正常鼻粘膜和24 例鼻息肉组织行免疫组化及 M G G 染色以观察嗜酸性粒细胞、单核细胞、巨噬细胞在组织中的分布程度。结果:鼻息肉组织中嗜酸性粒细胞、 C D68 阳性巨噬细胞和单核细胞显著增加。结论:鼻息肉的发生与炎性细胞的浸润、活化密切相关,药物治疗应是鼻息肉病治疗中的一个重要方面。 展开更多
关键词 鼻息肉 嗜酸性粒细胞 巨噬细胞 cd68抗原 病理
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