CD8~＋CD25~＋FOXP3~＋调节性T淋巴细胞在恶性胸腔积液中的表达及其临床意义

目的通过检测恶性胸腔积液中CD8＋CD25＋Foxp3＋调节性T淋巴细胞（T8reg）的表达,探讨其与恶性胸腔积液患者临床预后的关系。方法同步采集30例肺癌合并胸腔积液患者的胸腔积液和外周血,20例良性胸腔积液患者的胸腔积液和外周血,另采集20例健康对照者外周血,用流式细胞术检测上述标本中CD8＋CD25＋Foxp3＋T淋巴细胞的表型、百分比,分析其与恶性胸腔积液患者生存时间的关系。结果恶性胸腔积液组中T8reg占总CD8＋T细胞的比例显著高于良性胸腔积液组[（2.20±0.25）%vs（0.38±0.05）%,P=0.018],亦高于自身外周血组[（0.52±0.06）%,P=0.000],恶性胸腔积液患者外周血中T8reg的比例高于正常健康者外周血中的比例[（0.52±0.06）%vs（0.31±0.04）%,P=0.005]。而良性胸腔积液组胸腔积液、外周血（0.34±0.04）%与健康对照组外周血三组中T8reg细胞的数量占总CD8＋T细胞比例没有明显升高,差别没有统计学意义（P〉0.05）。T8reg高、低表达水平组患者的中位生存时间分别为105、195d,两者差异有统计学意义（P=0.004）。Cox回归模型多因素分析显示MPE中T8reg的表达水平、肿瘤大小是影响MPE患者预后的独立因素（P值分别为0.018、0.006）。结论肺癌伴胸膜转移患者的MPE及其外周血T8reg细胞的比例明显增高;MPE中T8reg细胞表达下降预示MPE患者生存率会明显改善,提示CD8＋CD25＋Foxp3＋T细胞在肺癌发生、发展的免疫病理过程中具有显著意义。     

肺癌患者外周血白细胞介素-17+CD4+T细胞和白细胞介素-17+CD8+T细胞表达的意义

目的 检测白细胞介素(IL)-17+CD4+T(Th17)细胞和IL-17+CD8+ T(Tc17)细胞在肺癌患者外周血中的表达水平,探讨二者在肺癌免疫中的作用及临床意义.方法 采用流式细胞术(FCM)检测60例肺癌患者及40例健康对照者外周血中Th17和Tc17细胞占CD;T细胞的比例.结果 肺癌组外周血中Th17细胞[(1.795±0.623)％]和Tc17细胞[(0.865±0.357)％]比例分别高于对照组[(1.405±0.256)％、(0.640±0.204)％],(t=28.944,P＜ 0.001;t=14.051,P＜ 0.001).两组内Th17细胞与Tc17细胞的表达水平均呈正相关(肺癌组r=0.770,P＜0.05;对照组r=0.532,P＜0.05).Th7细胞和Tc17细胞表达均与临床分期有关(F值分别为4.882、3.633,均P＜0.05),但与病理类型无关(均P＞0.05).结论 肺癌患者体内Th17细胞和Tc17细胞表达升高,二者可能参与了肺癌的发生、发展;Th17与Tc17细胞的表达水平可作为评价肺癌患者免疫功能状态的新指标,能为病情监测提供参考.     

DC-CIK对胃癌合并腹水患者外周血CD4+CD25+调节性T细胞增殖及功能的影响

目的:探讨DC-CIK对胃癌合并腹水患者外周血CD4+CD25+调节性T胞(Treg细胞)比例及功能的影响。方法:60例胃癌合并腹水患者,于输注DC-CIK前1天及DC-CIK治疗结束后1周分别采集外周血。流式细胞术检测外周血Treg细胞的比例,RT-PCR法检测其Foxp3mRNA表达情况;将分选出的Treg细胞和CD4+CD25-T细胞分为单纯Treg细胞组（A组）、1∶1混合培养（B组）、单纯CD4+CD25-细胞组（C组）进行培养,3H-TdR掺入法检测Treg细胞抑制CD4+CD25-细胞增殖的能力。结果:治疗后外周血Treg细胞占CD4+T细胞的比例较疗前显著下降［(6.21±1.37)% vs (9.38±1.06)%,P＜0.05］。治疗后Treg细胞Foxp3mRNA表达水平较治疗前显著下降［(56.18±13.25)% vs (85.26±11.58)%,P＜0.05］。治疗后Treg对CD4+CD25-T细胞抑制增殖能力较治疗前明显下降［(37.31±4.16)% vs (48.92±5.25)%,P＜0.05］。结论:输注DC-CIK免疫治疗,可显著降低胃癌合并腹水患者外周血Treg细胞比例,下调Foxp3mRNA表达水平,降低Treg细胞免疫抑制功能,有利于诱导抗肿瘤免疫效应。     

PD-1分子在肺癌恶性胸腔积液CD8+T细胞上的表达及其生物学意义

目的:观察肺癌恶性胸腔积液中CD8+T细胞上程序性死亡受体-1(programmed death-1, PD-1)分子的表达,并探讨其生物学意义.方法:通过免疫磁珠法从肺癌恶性胸腔积液中获得CD8+T细胞;采用FCM法检测CD8+T细胞上PD-1分子的表达;利用植物血凝素(phytohaemagglutinin,PHA)刺激CD8+T细胞反应体系,分别加入HEK293/PD-L1转基因细胞及空载体HEK293/mock细胞混合培养;FCM法分析CD8+T细胞表型的变化及细胞凋亡情况;ELISA法检测CD8+T细胞分泌干扰素-γ(interferon-γ,IFN-γ)水平的变化.结果:肺癌恶性胸腔积液中CD8+T细胞不同程度表达PD-1分子;PD-L1转基因细胞可显著抑制肺癌恶性胸腔积液中CD8+T细胞CD25的表达和IFN-γ的分泌,并诱导CD8+T细胞发生凋亡.结论:PD-1/PD-L1信号途径对肺癌恶性胸腔积液中CD8+T细胞的功能具有显著的负性调节作用,可能和肺癌细胞的免疫逃逸有关.     

晚期非小细胞肺癌患者外周血CD4~+ CD25~+ FOXP3~+调节性T细胞的表达及临床意义

目的探讨晚期非小细胞肺癌患者外周血CD4~+ CD25~+ FOXP3~+ 调节性T(Treg)细胞的表达及其临床意义。方法采用免疫荧光术及流式细胞仪检测50例晚期非小细胞肺癌患者及50例健康对照组外周血中CD4~+ CD25~+ FOXP3~+ Treg细胞、CD4~+ CD25~+ Treg细胞、CD4~+ T细胞和CD4~+ CTLA-4~+ T细胞的表达。结果晚期非小细胞肺癌患者外周血中CD4~+ CD25~+ FOXP3~+ Treg细胞、CD4~+ CD25~+ Treg细胞和CD4~+ CTLA-4~+ T细胞的比例均高于健康对照组(均P<0.05),CD4~+ T细胞的比例均低于健康对照组(均P<0.05)。结论晚期非小细胞肺癌患者外周血CD4~+ CD25~+ FOXP3~+ Treg细胞比例高于健康对照者,可能与肺癌患者的免疫抑制和肿瘤进展相关。     

GM-CSF 基因修饰肿瘤细胞疫苗治疗前后黑素瘤患者CD8 +T细胞的变化及其对预后的影响

目的:探讨粒细胞-巨噬细胞集落刺激因子(GM-CSF)基因修饰的肿瘤细胞疫苗(GM-CSF modified tumor cell vaccine,GVAX)治疗前后黑素瘤患者外周血免疫指标的变化及其对预后的影响。方法:收集2007年10月至2012年12月期间于天津医科大学肿瘤医院接受GVAX治疗的56例黑素瘤患者,采用流式细胞技术检测患者治疗前后外周血CD3+T细胞、CD4+T细胞、CD8+T细胞、调节性T细胞(Treg)、自然杀伤细胞(NK)及树突状细胞(DC1和DC2)的比例,分析治疗前后外周血各免疫细胞比例的变化,并探讨其与患者预后的关系。结果:GVAX治疗后患者外周血CD8+T细胞比例较前升高[(37.56±12.76)%vs(34.71±12.30)%,P=0.006],CD4+T细胞比例降低[(53.44±13.36)%vs(56.27±13.15)%,P=0.017],CD4+/CD8+比值降低[1.61(1.37)vs 1.75(0.71),P=0.009]。治疗后CD3+T、NK、Treg、DC1、DC2与治疗前的差异无统计学意义(P>0.05)。晚期患者GVAX治疗前外周血CD8+T细胞比例大于均值组与小于均值组相比,中位生存时间显著延长(29.16 vs 13.34个月,P=0.012)。结论:GVAX治疗黑素瘤可增强CD8+T细胞为主的抗肿瘤免疫应答,晚期患者外周血CD8+T细胞比例可作为预测GVAX疗效的指标,为判断预后起到一定的提示作用。     

鼻咽癌组织与外周血CD4+CD25+调节性T细胞检测及临床意义

目的 通过检测鼻咽癌患者肿瘤组织及外周血中CD4+T、CD8+T、CD4+CD25T、CD4+CD25+T细胞的频数,寻找客观、全面评价鼻咽癌患者免疫状态的临床指标.方法 采用流式细胞术检测40例初诊鼻咽癌患者及10例正常时照鼻咽部组织和外周血CD4+T、CD8+T、CD4+CD25-T、CD4+CD25+T细胞比例.结果 鼻咽癌患者CD4+T细胞比例及CD4+/CD8+T比值均低于对照组(P<0.05),而CD8+T细胞两组间差异无统计学意义(P>0.05),但是CD4+/CD8+T比值在鼻咽癌组织与外周血间差异无统计学意义(P>0.05).鼻咽癌组织及外周血中CD4+CD25+T细胞比例都高于对照组(P<0.05),同时癌组织中该细胞比例远远高于外周血(P<0.05).在鼻咽癌组织中CD4+CD25+T细胞与CD8+T细胞、CD4+CDQ5-T细胞呈负相关(r分别为-0.70、-0.675,P<0.05),而在外周血中没有相关关系(P>0.05).在不同T(原发肿瘤大小)组间,T4组的鼻咽癌组织中CD4+CD25+T细胞分别高于T1、T2、T3各组(P<0.05).而在T1、T2、T3各组间差异无统计学意义(P>0.05);鼻咽癌中CD4+CD25+T细胞比例与患者有无淋巴结转移并无关系(P>0.05);鼻咽癌组织中Ⅲ+Ⅳ期组CD4+CD25+T细胞比例高于Ⅰ+Ⅱ期组(P<0.05),而在外周血中两组间差异无统计学意义(P>0.05).结论 CD4+CD25+T细胞与鼻咽癌病程进展无相关性,但是联合检测患者肿瘤组织及外周血中CD4+CD25+T细胞的频数并结合既往CD4+/CD8+T比值会全面反应患者免疫状态,为临床治疗提供依据.     

健择联合顺铂化疗对非小细胞肺癌患者外周血CD4~+CD25~+Foxp3~+调节T细胞的影响

目的探讨健择联合顺铂对非小细胞肺癌患者免疫耐受的调控作用。方法38例经病理学或细胞学确诊的NSCLC患者,采用健择、顺铂联合化疗方案,应用流式细胞仪检测化疗前后外周血CD4+CD25+Foxp3+调节T细胞(Treg)占CD4+T细胞的百分率。结果化疗前NSCLC患者外周血CD4+CD25+Foxp3+调节T细胞(Treg)占CD4+T细胞的比率明显高于健康对照组(P<0.05);化疗后NSCLC患者外周血CD4+CD25+Foxp3+调节T细胞(Treg)占CD4+T细胞的百分率较化疗前显著降低(P<0.05);但鳞癌、腺癌及腺鳞癌3组间化疗前、化疗后各项指标之间差异无统计学意义(P>0.05)。结论健择联合顺铂化疗可调控晚期非小细胞肺癌机体的肿瘤免疫耐受,改善患者的免疫功能。     

CD+4 CD+25 调节性T细胞与急性髓细胞白血病关系的研究

 目的　探讨CD+4 CD+25 调节性T细胞（CD+4 CD+25 Treg细胞）在急性髓细胞白血病（AML）患者化疗前后外周血中的表达水平及其临床意义。方法　采用流式细胞术检测AML初发组（A组）、缓解3年内组（B组）、缓解3年以上组（C组）及正常对照组外周血中CD+4 CD+25 CDlow127 T细胞所占比例。结果　A组和B组外周血中CD+4 CD+25 Treg细胞比例均高于对照组（P＜0.05）;C组外周血CD+4 CD+25 Treg细胞比例与对照组相比差异无统计学意义（P＞0.05）;B组外周血中CD+4 CD+25 Treg细胞比例高于C组（P＜0.05）;A组外周血中CD+4 CD+25 Treg细胞比例明显高于B、C两组（P＜0.05）。结论　CD+4 CD+25 Treg细胞与AML发生有关,尤其与3年内容易复发密切相关。     

化疗对非小细胞肺癌患者外周血中CD8+CD28-T细胞表达的影响

目的 观察非小细胞肺癌(NSCLC)患者外周血中CD8+ CD28-T细胞的表达水平,研究化疗对CD8+ CD28-T细胞表达的影响及意义.方法 采用流式细胞仪检测70例初治NSCLC患者外周血CD8+ CD28-T细胞表达水平,以60例健康体检者作为对照,分析CD8+ CD28-T细胞与肺癌生物学及临床特征间的关系.观察30例NSCLC患者在给予长春瑞滨联合顺铂(NP)、吉西他滨联合顺铂(GP)两方案前后CD8+ CD28-T细胞表达的变化情况.结果 NSCLC患者CD8+ CD28-T细胞的表达率为(59.003±15.329)％,明显高于健康对照组(41.036±15.435)％,差异有统计学意义(t=35.904,P=0.001).CD8+ CD28-T细胞的表达与性别(F=1.374,P=0.697)、病理类型(F=0.779,P=0.509)及临床分期(F=0.070,P=0.933)无关,与年龄(F=15.038,P=0.001)有关.NP组化疗前后的CD8+ CD28-T细胞的表达率分别为(58.793±12.510)％和(55.293±14.637)％,差异有统计学意义(t=2.017,P=0.044).GP组化疗前后的CD8+ CD28-T细胞的表达率分别为(60.700±16.401)％和(54.127±13.924)％,差异有统计学意义(t=3.007,P=0.009).结论 CD8+ CD28-T细胞在NSCLC患者外周血中高表达,化疗可下调CD8+ CD28-T细胞的表达,为探讨NSCLC化疗联合免疫治疗提供了新的参考.     

CD4+CD25+调节性T细胞与CD4+T、CD8+T细胞在结直肠癌组织中的分布

 目的 分析CD4+CD25+ FOXP3+调节性T细胞（Treg）与CD4+T、CD8+T在结直肠癌（colorectal carcinoma, CRC）组织中的分布及其与临床病理特征之间的关系。方法 收集42例CRC新鲜手术标本,应用冰冻切片、免疫组织化学SP法检测肿瘤组织和癌旁组织中FOXP3+、CD4+T和CD8+T阳性细胞数。结果 CRC患者肿瘤组织中FOXP3表达水平显著升高,与癌旁组织相比差异有统计学意义（P<0.01）;中低分化组Treg细胞数明显高于高分化组（P<0.01）;淋巴结转移组Treg细胞数明显高于无淋巴结转移组（P<0.05）;癌巢内CD4+、CD8+T细胞数及CD4+/CD8+值显著低于间质（P<0.01）;Ⅲ+Ⅳ期、淋巴结转移组癌巢内CD4+/CD8+比值显著低于Ⅰ+Ⅱ期及无淋巴结转移组（P<0.05）;CRC中Treg数量与癌巢内CD4+/CD8+比值显著负相关（r=-0.605, P<0.01）。结论 CRC的发生发展可能与其癌组织局部微环境中Treg数量变化相关,肿瘤局部Treg数量的增多与T淋巴细胞亚群比例失调可能成为肿瘤免疫逃逸的机制之一。     

外周血CD3+、CD4+、CD8+、CD19+水平与喉癌患者预后的相关性

目的 探讨喉癌患者免疫水平的变化与病情进展的关系.方法 选取56例喉癌患者,用流式细胞仪检测不同分组的喉癌患者外周血淋巴细胞和NK细胞的表达水平.结果 手术后患者CD19+显著性下降(P＜0.05),而NK细胞显著上升(P＜0.05);有淋巴结转移的患者比无淋巴结转移的患者NK细胞上升,CD4+下降,二者均有统计学差异(P＜0.05);病理分期中Ⅲ～Ⅳ期的患者比Ⅰ～Ⅱ期表现出CD19+显著性下降(P＜0.05),CD4+则显著上升(P＜0.05).在术后随访18个月中,有复发或转移的患者比无转移且无复发患者CD4+下降,而NK细胞和CD19+上升,均具有统计学差异(P＜0.05).结论 喉癌患者免疫状态和病情之间有一定的联系.     

Epithelial mesenchymal transition correlates with CD24+CD44+ and CD133+ cells in pancreatic cancer

The epithelial-mesenchymal transition (EMT) has been linked to induction of a stem-cell like phenotype, characterized by altered cell surface marker expression and increased tumor formation. The aim of this study was to investigate whether EMT correlates with CD24+CD44+ and CD133+ cells in pancreatic cancer. The morphology of untreated and gemcitabine-treated SW1990 gemcitabine-resistant cells and normal SW1990 cells were compared. NF-κB p65 expression was knocked down using siRNA. Vimentin and E-cadherin expression were analyzed using western blotting, and CD24+CD44+, CD133+ cells were quantified by FACS. Additionally, immunohistochemistry of EMT-associated markers and stem cell-associated markers were performed in 41 cases of human pancreatic ductal adenocarcinoma. In SW1990 gemcitabine-resistant cells, gemcitabine induced a mesenchymal cell phenotype, expression of EMT-related molecular markers and increased CD24+CD44+ and CD133+ cells compared to untreated SW1990 gemcitabine-resistant and SW1990 cells. Knockdown of NF-κB p65 inhibited the ability of gemcitabine to increase the proportion of CD24+CD44+ or CD133+ cells and expression of EMT-related molecular markers. In human pancreatic ductal adenocarcinoma, significant correlations were observed between expression of the EMT-associated markers vimentin and E-cadherin, and stem cell-associated markers CD24, CD133 and CD44. This study demonstrated that EMT correlated with CD24+CD44+ and CD133+ cells in pancreatic cancer. This study also suggests that EMT may induce cancer stem-like cells in pancreatic cancer, with different degrees of EMT probability inducing different proportions of CD24+CD44+ and CD133+ cells.     

Immune surveillance: both CD3+ CD4+ and CD3+ CD8+ T cells control in vivo growth of P815 mastocytoma.

The aim of this study was to examine whether a spontaneous immune response controls neoplastic growth in P815-bearing DBA/2 mice, and to characterize the cells involved in tumor resistance in vivo. Several cell lineages such as T-cell-receptor (TcR)-bearing T cells, NK cells and macrophages mediate some anti-tumor activity in vitro. P815 was chosen as a model because it is weakly immunogenic and is a good target both for tumor-specific, MHC-restricted CTL-mediated lysis and for MHC-unrestricted lysis exerted by long-term cultured lymphocytes or activated macrophages. Since most "NK-like activity" in freshly isolated populations appears to be associated with CD3- cells, whereas antigen-specific, MHC-restricted T cells mostly express CD3 determinants, CD3 was a good marker for evaluating the role of T cells and "NK" cells in tumor resistance in vivo. The survival of anti-CD3-treated animals that were inoculated with tumor cells was strongly reduced (mean survival time: 17 days vs. 40 days for the control group) and was associated with increased tumor growth rate. We followed the same approach to define the T-cell subset(s) that mediate(s) this immune response. Both CD4+ and CD8+ T cells were required for induction of immune control on neoplastic growth. The approach used has revealed the important role of CD4+ T cells in immune responses that control in vivo growth of a class-I-positive, class-II-negative tumor and suggests that these cells may play a central role in tumor resistance. Since CD4+ cells are activated by soluble, exogenous proteins, this finding may have important implications for immunotherapy.     

CD4 + CD25 + 调节性T细胞与肿瘤免疫治疗

 CD4＋CD25＋调节性T淋巴细胞（regulatory Tcell，Treg）是一类具有独特免疫调节功能的T淋巴细胞亚群，一般占人外周血CD4＋T细胞的5％～15％。近年来，国内外对这类调节性T细胞的研究已从自身免疫耐受、移植免疫逐渐扩展到肿瘤免疫，认为Treg是形成肿瘤免疫耐受的关键成分。     

CD+4CD+25调节性T细胞与肿瘤免疫

 近期研究发现一个有独特免疫调节功能的T细胞亚群：CD+4 CD+25调节性T细胞,不仅能抑制自身免疫性疾病发生,还参与肿瘤免疫的调节。这群细胞具有免疫无能和免疫抑制特性,与肿瘤免疫逃逸有密切的关系。肿瘤环境中CD+4 CD+25调节性T细胞增加,导致肿瘤免疫失调,去除这群细胞可有效诱导肿瘤免疫,为肿瘤治疗提供了一种新的思路。     

CD4^＋CD25^＋调节性T细胞与肿瘤的相关性研究

通过了解CD4^＋CD25^＋调节性T细胞（CD4^＋CD25^＋Treg）表面分子的特性和CD4^＋CD25^＋Treg在外周血和组织中的表达,认识CD4^＋CD25^＋Treg在肿瘤免疫调节中的作用,探索其作用的分子机制。     

The impact of CD4+CD25+ Treg on tumor specific CD8+ T cell cytotoxicity and cancer

There is sufficient evidence to suggest that tumor growth elicits specific immune responses, including CD8(+) and CD4(+) T cell responses that may delay tumor growth and could potentially be harnessed to eradicate cancer. Nevertheless the frequent outcome of cancer is lethality associated with uncontrolled growth and dissemination of tumor cells. The failure of the immune response may be naturally programmed and related to a specific subpopulation of CD4(+)CD25(+) regulatory T cells, whose function is to protect us against autoimmunity. Recent investigations have shed light on the in vivo behavior and functions of these cells. It is becoming evident that a major impact of these cells is on the cytolytic action of specific CD8(+) T cells that target the tumor. Inhibition of cytotoxicity is dependent on TGF-beta signaling by the effector cells. Thus, targeting immune regulation may provide a promising approach to the immune therapy of cancer. This approach however could also have unexpected deleterious consequences, as surprising new observations indicate that regulatory T cells can also delay tumor growth by independent mechanisms that relate to their cross talk with the innate immune response to cancer.     

Co-immunization with L-Myc enhances CD8+ or CD103+ DCs mediated tumor-specific multi-functional CD8+ T cell responses

Renal carcinoma shows a high risk of invasion and metastasis without effective treatment. Herein, we developed a chitosan (CS) nanoparticle-mediated DNA vaccine containing an activated factor L-Myc and a tumor-specific antigen CAIX for renal carcinoma treatment. The subcutaneous tumor models were intramuscularly immunized with CS-pL-Myc/pCAIX or control vaccine, respectively. Compared with single immunization group, the tumor growth was significantly suppressed in CS-pL-Myc/pCAIX co-immunization group. The increased proportion and mature of CD11c⁺ DCs, CD8⁺CD11c⁺ DCs and CD103⁺CD11c⁺ DCs were observed in the splenocytes from CS-pL-Myc/pCAIX co-immunized mice. Furthermore, the enhanced antigen-specific CD8⁺ T lymphocyte proliferation, cytotoxic T lymphocyte (CTL) responses, and multi-functional CD8⁺ T cell induction were detected in CS-pL-Myc/pCAIX co-immunization group compared with CS-pCAIX immunization group. Of note, the depletion of CD8 T cells resulted in the reduction of CD8⁺ T cells or CD8⁺CD11c⁺ DCs and the loss of anti-tumor efficacy induced by CS-pL-Myc/pCAIX vaccine, suggesting the therapeutic efficacy of the vaccine was required for CD8⁺ DCs and CD103⁺ DCs mediated CD8⁺ T cells responses. Likewise, CS-pL-Myc/pCAIX co-immunization also significantly inhibited the lung metastasis of renal carcinoma models accompanied with the increased induction of multi-functional CD8⁺ T cell responses. Therefore, these results indicated that CS-pL-Myc/pCAIX vaccine could effectively induce CD8⁺ DCs and CD103⁺ DCs mediated tumor-specific multi-functional CD8⁺ T cell responses and exert the anti-tumor efficacy. This vaccine strategy offers a potential and promising approach for solid or metastatic tumor treatment.     

CD4+CD25+调节性T细胞与抗肿瘤免疫

CD4^＋CD25^＋调节性T（CD4^＋CD25^＋Tr）细胞是一类维持机体自身耐受的T细胞亚群,分布广泛,但不同组织表型有所不同。它们可由胸腺自然产生,也可在外周血中诱导产生,其活化要依赖于特异性抗原的存在。CD4^＋CD25^＋Tr细胞发挥抑制效应是通过细胞接触依赖或分泌细胞因子这两种方式。去除CD4^＋CD25^＋Tr细胞或抑制其功能,重新募集效应性T细胞能够增强机体抗肿瘤作用,这将成为一种可行的肿瘤免疫治疗方法。