胃癌患者外周血和肿瘤组织中高表达CD14+ DRlow/-髓源抑制性细胞

目的:探讨胃癌患者外周血和肿瘤组织中CD14+DRlow/-髓源抑制性细胞(myeloid-derived suppressor cells,MDSCs)的表达及其与肿瘤病理特征的关系。方法:选取2009年3月至2010年10月安徽医科大学第三附属医院胃癌患者43例(Ⅰ期9例、Ⅱ期13例、Ⅲ期14例、Ⅳ期7例),另采集26例正常健康者作为对照组。流式细胞术检测外周血、瘤组织中CD14+DRlow/-MDSCs的表达水平,分析MDSCs表达水平与肿瘤病理特征的相关性。结果:胃癌患者肿瘤组织中CD14+DRlow/-MD-SCs的表达显著高于自身外周和健康对照者外周血的表达水平[2.87±1.93)%vs(2.37±1.7)%,(0.89±0.47)%,P<0.05和P<0.01],后两者间差异也有统计学意义(P<0.01)。CD14+DRlow/-MDSCs的表达与胃癌的恶性程度呈正相关,晚期胃癌组织内CD14+DRlow/-MDSCs表达明显增加(Ⅰ∶Ⅱ∶Ⅲ∶Ⅳ=(1.15±0.78)%∶(1.71±0.92)%∶(2.25±1.24)%∶(4.85±2.37)%,P<0.05)。同时,肿瘤浸润组织与非浸润组织的CD14+DRlow/-MDSCs表达也有明显差异[3.90±1.67)%vs(2.62±1.53)%,P<0.05]。结论:CD14+DRlow/-MDSCs在胃癌患者外周血和肿瘤组织中均高表达,与胃癌的发生、发展密切相关。     

胃癌患者外周血CD4+ CD25highCD127low/-调节性T细胞表达临床意义分析

目的:研究CD4+CD25highCD127low/-调节性T细胞(Treg)在胃癌患者外周血中的表达水平,探讨其在肿瘤发病机制及治疗中的作用。方法:采用流式细胞术检测法检测90例胃癌患者(35例为早中期胃癌,55例为晚期胃癌)和30名健康体检者外周血中CD4+CD25highCD127low/-Treg的表达水平。结果:90例胃癌患者外周血CD4+T细胞中CD4+CD25highCD127low/-Treg含量为(11.60±5.99)%,高于健康体检者(5.19±1.72)%,t=5.610,P=0.007;Ⅲ+Ⅳ期患者外周血CD4+T细胞中CD4+CD25high CD127low/-Treg含量为(12.55±6.59)%,明显高于Ⅰ+Ⅱ期患者(10.39±4.68)%(t=4.113,P=0.04)和健康体检者(5.19±1.72)%(t=5.923,P=0.001)。手术后胃癌患者CD4+CD25highCD127low/-Treg水平为(6.12±2.13)%,明显低于手术前(11.25±5.63)%,t=5.237,P=0.04。结论:胃癌患者外周血CD4+CD25highCD127low/-Treg数量增多且与病程分期相关,手术后Treg数量明显减少,Treg可能参与了胃癌的发生发展。     

胃癌患者外周血CD4+CD25highCD127low/-调节性T细胞达临床意义分析

目的:研究CD4+ CD25high CD12low/-调节性T细胞(Treg)在胃癌患者外周血中的表达水平,探讨其在肿瘤发病机制及治疗中的作用.方法:采用流式细胞术检测法检测90例胃癌患者(35例为早中期胃癌,55例为晚期胃癌)和3(名健康体检者外周血中CD4+ CD25high CD127low/-Treg的表达水平.结果:90例胃癌患者外周血CD4+T细胞中CD4+CD25highCD127low/-Treg含量为(11.60±5.99)％,高于健康体检者(5.19±1.72)％,t=5.610,P=0.007;Ⅲ+Ⅳ期患者外周血CD4+T细胞中CD4+ CD25high CD127low/-Treg含量为(12.55±6.59)％,明显高于Ⅰ+Ⅱ期患者(10.39±4.68)％(t=4.113,P=0.04)和健康体检者(5.19±1.72)％(t=5.923,P=0.001).手术后胃癌患者CD4+ CD25high CD127low/-Treg水平为(6.12±2.13)％,明显低于手术前(11.25士5.63)％,t=5.237,P=0.04.结论:胃癌患者外周血CD4+ CD25highCD127low/-Treg数量增多且与病程分期相关,手术后Treg数量明显减少,Treg可能参与了胃癌的发生发展.     

喉鳞癌患者外周血CD45~(low)CD34~+KDR~+内皮祖细胞的检测及其临床意义

目的:研究喉鳞癌患者外周血中循环CD45lowCD34+KDR+内皮祖细胞(endothelial progenitor cells,EPCs)的水平及其与喉鳞癌发生、发展的相关性。方法:收集2010年2月至2011年2月20例喉鳞癌患者外周血标本,10例健康志愿者外周血作为对照。流式细胞术检测CD45lowCD34+KDR+EPCs占外周血CD34+造血干细胞或外周血淋巴细胞的比例,实时定量PCR检测PBMC中KDR mRNA和CD133 mRNA的表达水平,ELISA与Griess法分别检测血清中VEGF和NO的水平。结果:临床Ⅱ期~Ⅳ期的喉鳞癌患者外周血CD45lowCD34+KDR+EPCs占CD34+造血干细胞的比例和占淋巴细胞的比例均较健康对照组明显升高[(55.4±11.4)%vs(21.0±5.8)%,P<0.05;(1.27±0.25)vs(0.25±0.09),P<0.05]。临床Ⅱ期~Ⅳ期喉鳞癌患者PBMC中KDR mRNA和CD133 mRNA的表达水平及血清中VEGF水平均明显高于健康对照组(P<0.05),NO水平没有明显差异;而临床Ⅰ期的喉鳞癌患者CD45lowCD34+KDR+...     

胃癌患者术前血浆Big内皮素1水平检测的临床意义

背景与目的:内皮素是一种作用强大的血管收缩短肽,研究表明它还参与肿瘤细胞的分裂、凋亡、血管形成、侵袭与转移。Big内皮素1(Bigendothelin-1,Big ET-1)a是内皮素的前体物,具有更强的稳定性,常作为肿瘤进展与预后的标志物。本研究通过检测胃癌患者术前外周血中Big ET-1的水平及其蛋白在胃癌组织中的表达,探讨Big ET-1与胃癌的发展、术后复发和生存率的关系。方法:应用ELISA法检测118例胃癌患者及20例健康对照组的血浆BigET-1的水平。同时应用免疫组化法检测118例胃癌及癌旁组织中Big ET-1蛋白的表达。并分析其与胃癌术后复发和预后的关系。结果:进展期胃癌的血浆Big ET-1水平(5.78±1.85)ng/L显著高于早期胃癌的(3.13±1.72)ng/L(P=0.026)及健康对照组的(2.46±0.59)ng/L(P=0.008),早期胃癌与正常对照组间差异无统计学意义(P=0.086)。伴随淋巴结转移患者的血浆Big ET-1水平(6.13±2.34)ng/L显著高于无淋巴结转移者的(4.25±1.65)ng/L(P=0.006)。胃癌Ⅱ、Ⅲ、Ⅳ期患者Big ET-1水平显著高于Ⅰ期患者,但Ⅱ、Ⅲ、Ⅳ期者之间差异无统计学意义。胃癌患者术前Big ET-1高水平组的复发率(84.6%)显著高于较低水平组(60.9%)(P=0.034);其2年生存率较低水平组低(38.5%vs.56.5%,P=0.017)。Ⅱ、Ⅲ、Ⅳ期胃癌患者的Big ET-1蛋白阳性表达率显著高于Ⅰ期患者,Ⅱ、Ⅲ、Ⅳ期之间的差异无统计学意义。结论:胃癌患者术前血浆Big ET-1水平随肿瘤的进展而升高,与胃癌的发展、浸润及转移相关。术前血浆Big ET-1水平可作为判断胃癌患者病情程度及预后的一项指标。     

外周血单个核细胞采集术对肿瘤患者淋巴细胞亚群影响的观察

目的:探讨血细胞分离机采集恶性肿瘤患者外周血单个核细胞(简称"单采")对机体淋巴细胞亚群的影响。方法:采用流式细胞术(flow cytometry,FCM)检测105例恶性肿瘤患者(Ⅰ~Ⅲ期30例,Ⅳ期75例)单采前后和30名正常对照者外周血淋巴细胞亚群。结果:Ⅰ~Ⅲ期肿瘤患者CD4+细胞比例为(31.4±10.4)%,对照组为(39.6±6.3)%,差异有统计学意义,P=0.002;Ⅰ~Ⅲ期肿瘤患者CD3+CD56+细胞比例为(9.9±6.0)%,对照组为(13.4±5.7)%,差异有统计学意义,P=0.026;Ⅰ~Ⅲ期肿瘤患者CD4+/CD8+比值为1.2±0.7,对照组为1.6±0.4,差异有统计学意义,P=0.012。Ⅳ期肿瘤患者CD3+细胞比例为(64.0±9.3)%,CD4+为(28.4±9.2)%,CD4+/CD8+比值为1.1±0.6,与对照组比较均下降,P值均<0.001。Ⅰ~Ⅲ期肿瘤患者CD8+细胞比例为(30.5±11.6)%,Ⅳ期为(29.1±10.1)%,Ⅰ~Ⅲ期CD19+为(14.0±8.6)%,Ⅳ期为(17.4±8.3)%,Ⅰ~Ⅲ期CD4+CD25+为(3.8±1.6)%,Ⅳ期为(5.5±2.7)%,与对照组比较均上升,P值均<0.05。恶性肿瘤患者单采后第1天与单采前相比,淋巴细胞及单核细胞数下降,P值分别为0.048和0.035,血小板下降显著,P<0.001;单采后第3天与单采前相比,血常规各项指标无差异,淋巴细胞亚群中CD4+/CD8+比值略有下降,但差异无统计学意义,P=0.412;其余指标差异无统计学意义。结论:恶性肿瘤患者细胞免疫功能低下,随临床分期增加愈发明显;单采对恶性肿瘤患者血常规及细胞免疫影响是有限的。     

恶性肿瘤特异生长因子和肿瘤浸润性树突状细胞在子宫内膜癌患者中的表达及临床意义

目的:探讨恶性肿瘤特异生长因子(TSFG)和肿瘤浸润性树突状细胞(TIDC)在子宫内膜癌患者中的表达及临床意义。方法:选择2015年1月至2017年1月我院收治的子宫内膜癌患者50例。检测子宫内膜组织中TIDC和血清中TSFG水平,分析TSFG、TIDC在不同临床病理特征患者中的表达。结果:与癌旁组织比较,肿瘤组织中TIDC明显降低(P=0.000);MHC-Ⅱ阳性树突状细胞（DC）(%)明显降低（P=0.000);CD54阳性DC(%)明显降低（P=0.000)。与非淋巴结转移的患者相比,淋巴结转移的患者TIDC、MHC-Ⅱ阳性DC(%)、CD54阳性DC(%)均明显降低,TSFG明显增高(P<0.05)。与临床TNM分期为Ⅰ或Ⅱ期的患者相比,Ⅲ或Ⅳ期的患者TIDC、MHC-Ⅱ阳性DC(%)和CD54阳性DC(%)均明显降低,TSFG明显增高(P<0.05)。与肌层浸润≤1/2的患者相比,肌层浸润>1/2的患者TIDC、MHC-Ⅱ阳性DC(%)和CD54阳性DC(%)均明显降低,TSFG明显增高(P<0.05)。与中、高分化的患者相比,低分化患者组织中TIDC、MHC-Ⅱ阳性DC(%)和CD54阳性DC(%)均明显降低,TSFG明显增高（P<0.05）。结论:TIDC在肿瘤组织中低表达,且多为不成熟的调节性DC细胞。低分化、TNM分期为Ⅲ或Ⅳ期、淋巴结发生转移、肌层浸润>1/2的患者血清中TSFG水平明显升高,而肿瘤组织中TIDC明显降低。提示子宫内膜癌患者血清中TSFG和肿瘤组织中TIDC可作为判断预后的指标。     

口腔鳞癌患者IL-7和FOXp3的表达及临床意义

目的探讨口腔鳞癌患者外周血与癌组织中白细胞介素-7(IL-7)和FOXp3表达水平的差异。方法选取2013年8月至2015年8月间中国人民解放军第二五四医院经病理检查确诊的30例口腔鳞状细胞癌患者为试验组,同期来院行常规体检的30例健康人群为对照组。取两组人群外周血,检测IL-7及FOXp3水平,比较试验组患者不同病理分期口腔癌组织和癌旁组织中IL-7及FOXp3表达情况。结果相较于健康人外周血中的IL-7为(1.31±0.31)pg/ml和FOXp3表达量为单位1,Ⅰ~Ⅱ期和Ⅲ~Ⅳ期口腔癌患者外周血中IL-7为(16.32±4.53)pg/ml和(25.24±4.73)pg/ml,FOXp3为(5.12±3.03)和(12.42±4.11)呈明显高表达,差异均有统计学意义(均P<0.05),且IL-7和FOXp3表达水平呈明显正相关(r=0.742,P<0.05)。Ⅰ~Ⅱ期和Ⅲ~Ⅳ期口腔癌患者癌组织中IL-7为(19.75±5.64)pg/ml和(33.42±6.47)pg/ml,FOXp3为(8.04±4.21)和(22.41±5.37),表达量明显高于癌旁组织(1.35±0.24)pg/ml,差异均有统计学意义(均P<0.05),且Ⅲ~Ⅳ期口腔癌患者癌组织中IL-7(33.42±6.47)pg/ml和FOXp3(22.41±5.37)表达量较Ⅰ~Ⅱ期口腔癌患者癌组织中IL-7(19.75±5.64)pg/ml和FOXp3(8.04±4.21)表达量明显偏高,差异有统计学意义(P<0.05)。口腔癌组织中IL-7和FOXp3表达水平呈明显正相关(r=0.544,P<0.05)。结论 IL-7和FOXp3在口腔鳞癌患者癌组织和外周血中呈现明显的高表达,其表达水平与口腔癌的发生发展有一定相关性。     

大肠癌患者外周血CD4~+ CD25~+ CD127~-调节性T细胞表达及其临床意义

目的:探讨CD4+CD25+CD127-调节性T细胞在大肠癌患者外周血中的表达水平及临床意义。方法:应用流式细胞仪检测200例大肠癌患者外周血CD4+CD25+CD127-调节性T细胞占CD4+T细胞的百分比,并分析其与大肠癌组织的分化程度、淋巴结转移和临床分期的关系。结果:大肠癌患者外周血CD4+CD25+CD127-调节性T细胞占CD4+T细胞的百分率〔(4.84±1.35)%〕明显高于健康对照组〔(0.85±0.25)%〕,差异有统计学意义,P<0.05。低分化者外周血调节性T细胞〔(4.21±0.42)%〕明显高于高分化者〔(3.92±0.41)%〕,差异有统计学意义,P<0.05;有淋巴结转移者外周血调节T细胞〔(4.57±1.44)%〕明显高于无淋巴结转移者〔(2.36±0.68)%〕,差异有统计学意义,P<0.01;Ⅲ和Ⅳ期患者外周血调节性T细胞〔(3.53±1.41)%和(4.38±1.32)%〕明显高于Ⅰ～Ⅱ期〔(1.90±0.86)%〕,差异有统计学意义,P<0.01。结论:大肠癌患者外周血CD4+CD25+CD127调节性T细胞占CD4+T细胞的百分率明显升高,可能在大肠癌的免疫耐受和免...     

IL-6 通过诱导SOCS3表达缺失促进乳腺癌MDSCs 浸润和免疫抑制活性

目的：探讨髓系来源抑制细胞（myeloid-derived suppressor cells,MDSCs）通过IL-6 诱导STAT3/IDO信号通路活化对T细胞的免疫抑制作用及其分子机制。方法：收集天津医科大学肿瘤医院2015 年11 月至2016 年2 月收治的20 例乳腺癌患者肿瘤组织及其癌旁组织和40 例健康供者的外周血样本。免疫磁珠技术分选肿瘤组织中的CD33+和健康供者外周血中的CD33+和CD14+细胞,CD33+体外与乳腺癌细胞系MDA-MB-231 共孵诱导MDSCs生成。流式细胞术检测表型为CD45+CD13+CD33+CD14-CD15-的MDSCs 比例,Western blotting 检测细胞因子信号转导抑制因子1(suppressors of cytokine signalling 1,SOCS1)、SOCS3、JAK1、JAK2、TYK2、STAT1、STAT3 及其磷酸化水平,qRT-PCR 检测IL-6、SOCS1-3 的表达水平,CCK-8 法检测T 细胞增殖情况,Annexin V检测T 细胞凋亡,ELISA 检测T 细胞分泌的IL-10 和IFN-γ。结果：20 例乳腺癌组织中均有不同程度的MDSCs浸润（15.3%~58.1%）,平均为（29.82±11.46）%;IL-6high组MDSCs浸润比例明显高于IL-6low组[ （13.75±3.44）% vs（4.31±1.50）%,P<0.05],且IL-6 表达与MDSCs浸润呈正相关（R2=0.4399,P<0.01)。体外实验发现肿瘤源性IL-6 明显促进体外MDSCs的生成和免疫抑制活性,该过程可被IL-6 信号的阻断所逆转（P<0.05）;同样发现在体外诱导的MDSCs中SOCS3 表达缺失,阻断IL-6 后,以上过程被明显抑制（P< 0.05）。结论：乳腺癌来源的IL-6 刺激MDSCs中JAK/STAT信号通路的持续活化和SOCS3 的表达缺失,进而促进MDSCs的浸润、生成和免疫活性。因此IL-6 信号通路可以作为削弱MDSCs生成和逆转MDSCs活性的治疗靶点。     

Immune selection in neoplasia: towards a microevolutionary model of cancer development

The dual properties of genetic instability and clonal expansion allow the development of a tumour to occur in a microevolutionary fashion. A broad range of pressures are exerted upon a tumour during neoplastic development. Such pressures are responsible for the selection of adaptations which provide a growth or survival advantage to the tumour. The nature of such selective pressures is implied in the phenotype of tumours that have undergone selection. We have reviewed a range of immunologically relevant adaptations that are frequently exhibited by common tumours. Many of these have the potential to function as mechanisms of immune response evasion by the tumour. Thus, such adaptations provide evidence for both the existence of immune surveillance, and the concept of immune selection in neoplastic development. This line of reasoning is supported by experimental evidence from murine models of immune involvement in neoplastic development. The process of immune selection has serious implications for the development of clinical immunotherapeutic strategies and our understanding of current in vivo models of tumour immunotherapy.     

Opposite immune functions of GM-CSF administered as vaccine adjuvant in cancer patients.

Granulocyte-macrophage colony-stimulating factor (GM-CSF) has been and is still widely used as an adjuvant in clinical trials of vaccination with autologous tumor cells, peptides and/or dendritic cells in a variety of human neoplasms. This cytokine was administered either as product of gene-transduced tumor cells or as recombinant protein together with the vaccine given subcutaneously or intradermally. Results of these trials were heterogeneous in terms of induction of vaccine-specific immune response and of clinical response. Though in some of these studies GM-CSF appeared to help in generating an immune response, in others no effect or even a suppressive effect was reported. Here, we review the literature dealing with the immune adjuvant activity of GM-CSF both in animal models and clinical trials. As a consequence of such analysis, we conclude that GM-CSF may increase the vaccine-induced immune response when administered repeatedly at relatively low doses (range 40-80 microg for 1-5 days) whereas an opposite effect was often reported at dosages of 100-500 microg. The potential mechanisms of the GM-CSF-mediated immune suppression are discussed at the light of studies describing the activation and expansion of myeloid suppressor cells by endogenous tumor-derived or exogenous GM-CSF.     

依赖NKG2D的肿瘤免疫逃避

活化性受体NKG2D（natural—killer group 2,member D）和其配基在NK、γδ^＋T和CD8^＋T细胞介导的肿瘤免疫应答中扮演了重要角色。NKG2D识别肿瘤细胞表面的配体激活效应细胞,产生有效的抗肿瘤免疫应答。但是在完全具有免疫能力的机体内,表达NKG2D配基的肿瘤仍能够生长发育,因此,在患肿瘤小鼠和肿瘤病人中一定存在着依赖NKG2D的免疫逃避机制。本文就依赖于NKG2D的免疫逃避作一详细综述,主要包括：干涉NKG2D受体的免疫逃避、干涉NKG2D配基的免疫逃避、细胞因子破坏NKG2D受体和配基的免疫逃避、抑制性细胞参与NKG2D介导的免疫逃避。这些研究为抗肿瘤治疗提供了新的途径。     

Septic arthritis: a complication of BCG immunotherapy.

A new complication of cutaneous vaccination for immune therapy is reported: non-acid-fast bacteremia with metastatic septic arthritis. Systemic antibiotics should be administered prophylactically in patients with signs and symptoms of local infection, particularly in the presence of orthopedic prostheses or valvular heart disease.     

恶性肿瘤患者红细胞免疫功能及CR1免疫调节功能的观察

目的观察恶性肿瘤患者红细胞免疫功能及其血清中Ⅰ型补体受体(CR1)免疫调节因子活性的变化.方法采用红细胞-酵母菌免疫粘附法,测定137例恶性肿瘤患者红细胞免疫功能及其血清中CR1免疫调节功能.结果恶性肿瘤患者的红细胞C3b受体花环率(13.37%±2.86%)与对照组(18.50%±2.65%)相比,显著降低(P＜0.01),红细胞免疫复合花环率(10.15%±2.08%)与对照组(6.84%±1.55%)相比,显著增高(P＜0.01),CR1免疫粘附促进因子活性(130.98%±28.34%)与对照组(189.06%±28.28%)相比,显著降低(P＜0.01),而CR1免疫粘附抑制因子活性(46.72%±9.38%)与对照组(34.64%±7.99%)相比,显著增高(P＜0.01).结论红细胞免疫功能的检测对恶性肿瘤的诊断、疗效观察、预后判断有一定的应用价值.     

Pyroptosis,a new bridge to tumor immunity

Pyroptosis refers to the process of gasdermin (GSDM)-mediated programmed cell death (PCD). Our understanding of pyroptosis has expanded beyond cells and is known to involve extracellular responses. Recently, there has been an increasing interest in pyroptosis due to its emerging role in activating the immune system. In the meantime, pyroptosis-mediated therapies, which use the immune response to kill cancer cells, have also achieved notable success in a clinical setting. In this review, we discuss that the immune response induced by pyroptosis activation is a double-edged sword that affects all stages of tumorigenesis. On the one hand, the activation of inflammasome-mediated pyroptosis and the release of pyroptosis-produced cytokines alter the immune microenvironment and promote the development of tumors by evading immune surveillance. On the other hand, pyroptosis-produced cytokines can also collect immune cells and ignite the immune system to improve the efficiency of tumor immunotherapies. Pyroptosis is also related to some immune checkpoints, especially programmed death-1 (PD-1) or programmed death- ligand 1 (PD-L1). In this review, we mainly focus on our current understanding of the interplay between the immune system and tumors that process through pyroptosis, and debate their use as potential therapeutic targets.     

Is the skin a sanctuary for breast cancer cells during treatment with anti-HER2 antibodies?

The occurrence of skin metastases is a common event in patients affected by advanced breast cancer, usually associated with systemic disease progression. Here we describe 2 cases of diffuse cutaneous metastases from HER2-overexpressing breast cancer occurring despite a dramatic response in liver and bone, respectively, during treatment with anti-HER2 antibodies Trastuzumab and Pertuzumab. We discuss the reasons for this discrepancy and suggest a possible implication of impaired immune response in the skin. Future research should provide strategies to overcome the induction of immune privilege in the skin in order to avoid discontinuation of effective treatments.     

Regulatory T (Treg) cells in cancer: Can Treg cells be a new therapeutic target?

Regulatory T (Treg) cells suppress abnormal/excessive immune responses to self‐ and nonself‐antigens to maintain immune homeostasis. In tumor immunity, Treg cells are involved in tumor development and progression by inhibiting antitumor immunity. There are several Treg cell immune suppressive mechanisms: inhibition of costimulatory signals by CD80 and CD86 expressed by dendritic cells through cytotoxic T‐lymphocyte antigen‐4, interleukin (IL)‐2 consumption by high‐affinity IL‐2 receptors with high CD25 (IL‐2 receptor α‐chain) expression, secretion of inhibitory cytokines, metabolic modulation of tryptophan and adenosine, and direct killing of effector T cells. Infiltration of Treg cells into the tumor microenvironment (TME) occurs in multiple murine and human tumors. Regulatory T cells are chemoattracted to the TME by chemokine gradients such as CCR4‐CCL17/22, CCR8‐CCL1, CCR10‐CCL28, and CXCR3‐CCL9/10/11. Regulatory T cells are then activated and inhibit antitumor immune responses. A high infiltration by Treg cells is associated with poor survival in various types of cancer. Therefore, strategies to deplete Treg cells and control of Treg cell functions to increase antitumor immune responses are urgently required in the cancer immunotherapy field. Various molecules that are highly expressed by Treg cells, such as immune checkpoint molecules, chemokine receptors, and metabolites, have been targeted by Abs or small molecules, but additional strategies are needed to fine‐tune and optimize for augmenting antitumor effects restricted in the TME while avoiding systemic autoimmunity. Here, we provide a brief synopsis of these cells in cancer and how they can be controlled to achieve therapeutic outcomes.     

HBV感染肝癌患者血清中Ig和CIC的检测与研究

目的了解HBV感染肝癌患者血清中Ig和CIC含量。方法用速率散射比浊法对正常组与HBV感染肝癌组以及HBV阴性肝癌组进行对比。结果肝癌患者与对照组相比前者血清中Ig和CIC含量明显升高(P<0.05),HBV感染肝癌患者与阴性肝癌患者相比前者血清中Ig和CIC含量明显升高(P<0.05)。结论肝癌患者由于HBV的感染,病毒复制时伴有血清Ig、CIC升高,是病情危险的信号,要紧密观察患者,采取必要的救治措施。