冷冻消融对肝癌患者外周血CD4+CD25+调节T细胞影响的初步研究

目的探讨氩氦冷冻对肝癌外周血CD4 CD25 调节T细胞的影响及临床意义.方法原发性肝癌患者20例.其中Ⅱ期14例、Ⅲ期6例,分别采集氩氦冷冻治疗术前及术后1个月外周血,采用流式细胞术检测外周血T淋巴细胞亚群(CD3 T、CD4 T、CD8 T、CD4 T/CD8 T、NK细胞)及Treg细胞.结果肝癌Ⅲ期患者外周血Treg细胞占CD4 T细胞比例明显高于Ⅱ期患者(6.5%±1.2%、9.1%±2.0%,P=0.013).与氩氦冷冻治疗前比较治疗后1个月Treg细胞一定程度降低(8.2%±1.1%、7.7%±1.0%),但差异无显著性(P=0.052);CD4 T、CD4 T/CD8 T、NK细胞明显升高,CD8 T细胞降低(P＜0.05).结论肿瘤负荷可显著促进肝癌患者外周血Treg细胞分化.肝癌氩氦冷冻治疗后短期内Treg细胞比例轻度下降,T淋巴细胞亚群分布异常得到一定改善.     

氩氦冷冻消融对晚期肾癌外周血调节性T 细胞的影响*

目的:研究氩氦冷冻消融治疗对晚期肾癌患者外周血CD4 +CD 25+ 调节性T 细胞（Treg ）的影响及临床意义。方法:回顾性分析本院32例晚期肾癌患者临床资料,所有患者均于氩氦冷冻消融治疗术前、术后1～6 个月分别取外周血,应用流式细胞仪检测外周血T 淋巴细胞亚群（CD3 + T、CD4 + T、CD8 + T、CD4 +T/CD 8 +T、NK细胞、Treg 细胞）变化情况。术后1 个月采用增强MRI或CT评价肿瘤坏死情况,影像学显示肿瘤无强化区即认为肿瘤坏死,根据Cavalieri 方法计算肿瘤坏死率,进而评价肿瘤负荷。结果:冷冻消融治疗术后,Treg 细胞比例由术前（4.18± 1.58）% 逐渐下降至第3 个月达最低值（1.96± 0.54）% ,二者差异有统计学意义（P=0.001）。 CD3 +T、CD4 +T、CD4 +T/CD 8 +T、NK细胞比例分别由术前（19.26± 7.52）% 、（43.54± 12.99）% 、（1.15± 0.57）% 、（17.49±8.36）% 逐渐上升至第3 个月达最大值（30.83± 5.69）% 、（49.58± 10.76）% 、（1.84± 0.12）% 、（27.63± 8.20）% ,差异均有统计学意义（P=0.000,P=0.003,P=0.02,P=0.001）。 CD8 + T由术前（40.86± 8.89）% 逐渐下降至第3 个月达最低值（26.74± 4.29）% ,差异具有统计学意义（P=0.000）。 冷冻治疗后3～6 个月CD3 +T、CD4 +T、CD4 +T/CD 8 +T、NK、CD8 + T、Treg 细胞比例虽略有改变但差异均无统计学意义（P>0.05）。相关性分析结果表明:经氩氦冷冻治疗后Treg 细胞比例变化与肿瘤负荷下降程度呈正相关（r=0.793,P<0.01）。结论:肾癌氩氦冷冻治疗后外周血T 淋巴细胞亚群分布异常得到一定改善,抗肿瘤免疫反应增强,Treg 细胞比例变化与肿瘤负荷有关。      

化疗对鼻型NK/T细胞淋巴瘤患者细胞免疫功能的影响

目的:通过对鼻型NK/T细胞淋巴瘤患者化疗前、后外周血T 淋巴细胞各亚群及NK细胞检测来探讨化疗对其细胞免疫功能的影响。方法:分组对照研究,鼻型NK/T细胞淋巴瘤患者（实验组）41例,分别在化疗前及化疗2 个周期结束后10d 两次检测外周血T 淋巴细胞各亚群及NK细胞数目。正常健康组35例（对照组）。 对相关实验结果进行统计学分析。结果:鼻型NK/T细胞淋巴瘤患者化疗前与正常健康组相比,T 淋巴细胞亚群比例紊乱,CD3+、CD4+比例和CD4+/CD 8+比值及NK细胞明显下降,CD8+比例及CD4+CD25+调节性T 细胞（Tregulatory cells ,Treg ）明显升高（P<0.05）。 经过2 个周期的化疗治疗,化疗有效组化疗后CD3+、CD4+比例、NK细胞比例、CD4+/CD 8+比化疗前明显升高（P<0.05）,CD8+比例、CD4+CD25+Treg 明显下降（P<0.05）。 化疗有效组化疗后除CD4+、CD8+比例外,其他指标与正常健康组相比差别均无统计学意义（P>0.05）;而无效组患者化疗后CD4+比例、CD8+比例、CD4+/CD 8+比值、NK细胞数目比化疗前则进一步下降（P<0.05）。 结论:鼻型NK/T细胞淋巴瘤患者细胞免疫功能低下,T 淋巴细胞亚群比例紊乱,NK细胞明显下降。有效化疗可通过杀伤、诱导肿瘤细胞凋亡,减轻肿瘤负荷,减少CD4+CD25+Treg ,排除某些免疫抑制因素;改善了患者的细胞免疫功能,化疗无效患者其细胞免疫功能则继续恶化。通过检测患者的T 淋巴细胞各亚群及NK细胞数变化可以反映患者的细胞免疫功能状态,对指导临床治疗、判断预后有重要的意义。      

化疗对肺癌患者外周血中CD4~＋ CD25~＋调节性T细胞数目的影响及意义

目的研究化疗药物对肺癌患者外周血中Treg（CD4＋ CD25＋调节性T细胞）的影响及意义。方法采集60例肺癌术后患者化疗前1天及化疗后第10天外周静脉血,应用流式细胞技术检测外周血中Treg细胞以及CD3＋、CD4＋、CD8＋T、NK细胞占T淋巴细胞百分比,CD4＋T/CD8＋T比值。结果化疗前NSCLC患者外周血CD4＋ CD25＋调节T细胞比率明显高于健康对照组（P〈0.05）;且Ⅳ期患者调节T细胞比率明显高于Ⅲ期患者（P〈0.05）。化疗后NSCLC患者外周血CD4＋ CD25＋调节T细胞较化疗前显著降低（P〈0.05）。化疗前后不同病理分型患者外周血中CD4＋CD25＋细胞变化差异无统计学意义。化疗后CD8＋T细胞占T淋巴细胞比例（28.129±10.900）%较化疗前（24.876±6.631）%升高（P〈0.05）。化疗后CD4＋/CD8＋（1.506±0.691）较化疗前（1.680±0.704）降低（P〈0.05）。结论肿瘤负荷可显著促进肺癌患者外周血Treg细胞分化,化疗后肺癌患者Treg细胞比例下降。     

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.     

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。     

急性白血病患者外周血淋巴细胞亚群和调节性T细胞的检测及临床意义

目的:研究急性白血病患者外周血淋巴细胞亚群、调节性T细胞水平的变化及临床意义.方法: 采用流式细胞仪对60例急性白血病(AL)患者[急性髓细胞性白血病(AML)30例、急性淋巴细胞性白血病(ALL)30例]及40例正常人外周血淋巴细胞亚群及调节性T细胞水平进行检测.结果: 初诊AL组与正常对照组比较,CD3+ T淋巴细胞百分比、CD4+T淋巴细胞百分比、CD4+/CD8+ 比值及CD16+/56+ NK细胞百分比均明显降低( P<0.05) ;CD8+ T 淋巴细胞百分比与CD19+ B淋巴细胞百分比均明显升高(P均 <0.01).ALL组CD4+T淋巴细胞百分比及CD4+/CD8+ 比值明显低于AML组( P<0.01).与对照组相比较,初诊AL患者外周血CD4+CD25+ T细胞和CD4+CD25high Treg 细胞均明显升高(P<0.01).结论: AL患者细胞免疫功能明显异常;与AML患者相比,ALL患者细胞免疫功能更为低下.CD4+CD25 high Treg细胞增多可能是AL患者免疫功能受抑的重要原因之一.淋巴细胞亚群及调节性T细胞水平检测在评价AL疗效及判断预后方面具有一定的临床价值.     

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。     

小儿急性淋巴细胞白血病血清CD3+ CD4- CD8- T细胞和T细胞亚群的变化及其临床意义

目的 探讨小儿急性淋巴细胞白血病(ALL)外周血CD3+ CD4- CD8- T细胞(DNT细胞)及T淋巴细胞亚群的变化及意义.方法 采用免疫荧光流式细胞术检测30例ALL患儿及24例健康小儿外周血DNT细胞及T淋巴细胞亚群CD3+ T细胞、CD3+ CD4+ T细胞及CD3+ CD8+ T细胞水平.结果 DNT细胞、CD3+ T细胞、CD3+ CD4+ T细胞百分比均明显低于对照组,分别为(4.93±3.75)%比(8.19±3.21)%(t=3.4,P<0.01):(49.99 ±11.70)%比(64.13 ±11.39)%(t=4.1,P<0.01);(28.30 ±7.56)%比(34.61 ±6.43)%(t=3.2,P<0.01);而CD3+ CD8+ T细胞百分比明显高于对照组,为(31.19±9.89)%比(24.33 ±4.24)%(t=3.1,P<0.01).结论 ALL患儿外周血DNT细胞及T亚群的变化提示患儿体内存在免疫功能紊乱,这可能与ALL的发病机制有关.     

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.     

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.     

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.     

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.     

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。     

Ex vivo expansion of CD8+CD56+ and CD8+CD56- natural killer T cells specific for MUC1 mucin

Prostate cancers express MUC1, but nearly all metastatic cells lack HLA class I molecules. Thus, a lymphocyte population that can sense its antigenic environment, while also able to react to stimuli of natural killer (NK) cells, may be a more versatile effector cell population for antitumor immune responses. Herein, we report that tumor-specific MUC1 peptide, interleukin 2, and interleukin 12 act synergistically to stimulate the ex vivo expansion of CD8(+)CD56(-) T cells and CD8(+)CD56(+) natural killer T (NKT) cells from the peripheral blood mononuclear cells of prostate cancer patients, as well as healthy male and female donors. Both the CD56(+) NKT cells and CD56(-) T cells lysed allogeneic mucin-bearing target cells, as well as NK target cells, but not lymphokine-activated killer target cells. However, the CD56(+) NKT cells displayed a 2-fold greater cytolytic activity than the CD56(-) T cells. The mucin-specific cytolytic activity and NK cytolytic activities for both lymphocyte populations were independent of HLA class I and CD1 molecules. The CD56(-) T cells up-regulated CD56 with continued antigenic stimulation in the presence of interleukin 12, suggesting that CD8(+)CD56(-) T cells are NKT cells. However, CD56(+) NKT cells expand poorly to continued stimulation. All mucin-stimulated NKT cells exhibited the activated/memory CD45RO phenotype. The NKT cell lines express the alpha/beta T-cell receptor (TCR). The TCR repertoire was limited and varied with cell line, but was not the V alpha 24V beta 11 TCR typically associated with NKT cells. Whereas CD161 is generally considered a marker of NKT cells, the mucin-stimulated NKT cells did not express this marker. Thus, we have described two phenotypically distinct NKT types that do not display a biased TCR repertoire, but do display specificity for a tumor-specific peptide antigen (CTL-like activity), as well as HLA class I-deficient target cells (NK-like activity).