Natural killer cells in tumor immunotherapy

Cancer is the second most common cause of death worldwide and remains one of the critical public health problems of our time1.Recently,immunotherapy has considerably improved the outcomes of patients with advanced cancers.Immune checkpoint blockade and chimeric antigen receptor(CAR)-T cell-based therapies have achieved remarkable success in recent decades,thus placing the host immune response in the spotlight as a potential new approach in antitumor therapy.

Immune evasion and therapeutic opportunities based on natural killer cells

Natural killer(NK)cells can elicit an immune response against malignantly transformed cells without recognizing antigens,and they also exhibit cytotoxic effects and immune surveillance functions in tumor immunotherapy.Although several studies have shown the promising antitumor effects of NK cells in immunotherapy,their function is often limited in the tumor microenvironment because tumor cells can easily escape NK cell-induced death.Thus,for efficient tumor immunotherapy,the mechanism by which tumor cells escape NK cell-induced cytotoxicity must be fully understood.Various novel molecules and checkpoint receptors that mediate the disruption of NK cells in the tumor microenvironment have been discovered.In this review,we analyze and detail the major activating and inhibitory receptors on the surface of NK cells to delineate the mechanism by which tumor cells suppress NKG2D ligand expression and increase tumor receptor and inhibitory receptor expression[NKG2A,programmed cell death1(PD-1),and T-cell immunoglobulin and immunoreceptor tyrosine inhibitory motif(TIGIT)]on the NK cell surface,and thus inhibit NK cell activity.We also reviewed the current status of treatments based on these surface molecules.By comparing the therapeutic effects related to the treatment status and bypass mechanisms,we attempt to identify optimal single or combined treatments to suggest new treatment strategies for tumor immunotherapy.

Designing a risk prognosis model based on natural killer cell-linked genes to accurately evaluate the prognosis of gastric cancer

Background:This study was aimed at identifying natural killer(NK)cell-related genes to design a risk prognosis model for the accurate evaluation of gastric cancer(GC)prognosis.Methods:We obtained NK cell-related genes from various databases,followed by Cox regression analysis and molecular typing to identify prognostic genes.Various immune algorithms and enrichment analyses were used to investigate the mutations,immune status,and pathway variations among different genotypes.The key prognostic genes were assessed using the least absolute shrinkage and selection operator(Lasso)regression analysis and univariate Cox regression analysis.Thereafter,the risk score(RS)prognosis model was constructed based on the selected important prognostic genes.A Receiver Operating Characteristics(ROC)curve was plotted for analyzing the robustness of the model.Subsequently,the decision and calibration curves were used for assessing the reliability and prediction accuracy of the proposed model.The‘pRRophetic’R software package was utilized for predicting the half-maximal inhibitory concentration(IC50)of immunotherapy and chemotherapy drugs.Results:We screened 21 prognostic genes and three molecular subtypes and found that the C1 subtype had the worst prognosis.Further,the pathways promoting tumor proliferation,such as epithelial-mesenchymal transition were significantly up-regulated.The results also showed that the macrophages in the M2 stage were significantly infiltrated in the C1 subtype,and there was significant overexpression in the C1 subtype,accompanied by a severe inflammatory reaction.The C1 was highly sensitive to drugs like 5-fluorouracil and paclitaxel.The ROC,calibration curve,and decision curve showed that the risk model was robust and strongly reliable.Conclusion:Overall,our proposed NK cell-related RS model can be used as a more accurate prediction index for GC patients,providing a valuable contribution to personalized medicine.

Establishment of a prognostic model related to tregs and natural killer cells infiltration in bladder cancer

BACKGROUND Regulatory T cells(Tregs)and natural killer(NK)cells play an essential role in the development of bladder urothelial carcinoma(BUC).AIM To construct a prognosis-related model to judge the prognosis of patients with bladder cancer,meanwhile,predict the sensitivity of patients to chemotherapy and immunotherapy.METHODS Bladder cancer information data was obtained from The Cancer Genome Atlas and GSE32894.The CIBERSORT was used to calculate the immune score of each sample.Weighted gene co-expression network analysis was used to find genes that will have the same or similar expression patterns.Subsequently,multivariate cox regression and lasso regression was used to further screen prognosis-related genes.The prrophetic package was used to predict phenotype from gene expression data,drug sensitivity of external cell line and predict clinical data.RESULTS The stage and risk scores are independent prognostic factors in patients with BUC.Mutations in FGFR3 lead to an increase in Tregs percolation and affect the prognosis of the tumor,and additionally,EMP1,TCHH and CNTNAP3B in the model are mainly positively correlated with the expression of immune checkpoints,while CMTM8,SORT1 and IQSEC1 are negatively correlated with immune checkpoints and the high-risk group had higher sensitivity to chemotherapy drugs.CONCLUSION Prognosis-related models of bladder tumor patients,based on Treg and NK cell percolation in tumor tissue.In addition to judging the prognosis of patients with bladder cancer,it can also predict the sensitivity of patients to chemotherapy and immunotherapy.At the same time,patients were divided into high and low risk groups based on this model,and differences in genetic mutations were found between the high and low risk groups.

Diffuse large B-cell lymphoma successfully treated with amplified natural killer therapy alone: A case report

BACKGROUND The prognosis of patients with advanced diffuse large B-cell lymphoma(DLBCL)is poor,with a 5-year survival rate of approximately 50%.The mainstay of treatment is multidrug combination chemotherapy,which has been associated with serious side effects.Amplified natural killer(ANK)cell therapy amplifies and activates natural killer(NK)cells to attack only malignant tumors.As ANK cells attack programmed death ligand 1(PD-L1)-positive tumor cells,ANK therapy is considered effective against adult T-cell lymphoma and malignant lymphoma.CASE SUMMARY Herein,we report a case of an older patient with advanced DLBCL who was successfully treated with ANK immunotherapy.A 91-year-old female visited our hospital with sudden swelling of the right axillary lymph node in April 2022.The patient was diagnosed with stage II disease,given the absence of splenic involvement or contralateral lymphadenopathy.ANK therapy was administered.Six rounds of lymphocyte sampling were performed on July 28,2022.To reduce the occurrence of side effects,the six samples were diluted by half to obtain 12 samples.Cultured NK cells were administered twice weekly.The treatment efficacy was evaluated by performing computed tomography and serological tests every 1 or 2 mo.The treatment suppressed lesion growth,and the antitumor effect persisted for several months.The patient experienced mild side effects.PD-L1 immunostaining was positive,indicating that the treatment was highly effective.CONCLUSION ANK therapy can be used as a first-line treatment for malignant lymphoma;the PD-L1 positivity rate can predict treatment efficacy.

Intestinal natural killer/T-cell lymphoma presenting as a pancreatic head space-occupying lesion:A case report

BACKGROUND Intestinal natural killer/T-cell lymphoma(NKTCL)is a rare and aggressive non-Hodgkin’s lymphoma,and its occurrence is closely related to Epstein-Barr virus infection.In addition,the clinical symptoms of NKTCL are not obvious,and the specific pathogenesis is still uncertain.While NKTCL may occur in any segment of the intestinal tract,its distinct location in the periampullary region,which leads clinicians to consider mimics of a pancreatic head mass,should also be addressed.Therefore,there remain huge challenges in the diagnosis and treatment of intestinal NKTCL.CASE SUMMARY In this case,we introduce a male who presented to the clinic with edema of both lower limbs,accompanied by diarrhea,and abdominal pain.Endoscopic ultrasound(EUS)showed well-defined homogeneous hypoechoic lesions with abundant blood flow signals and compression signs in the head of the pancreas.Under the guidance of EUS-fine needle biopsy(FNB)with 19 gauge or 22 gauge needles,combined with multicolor flow cytometry immunophenotyping(MFCI)helped us diagnose NKTCL.During treatments,the patient was prescribed the steroid(dexamethasone),methotrexate,ifosfamide,L-asparaginase,and etoposide chemotherapy regimen.Unfortunately,he died of leukopenia and severe septic shock in a local hospital.CONCLUSION Clinicians should enhance their understanding of NKTCL.Some key factors,including EUS characteristics,the right choice of FNB needle,and combination with MFCI,are crucial for improving the diagnostic rate and reducing the misdiagnosis rate.

非小细胞肺癌患者血清CA211水平和NK细胞数与预后相关

目的 探究非小细胞肺癌(NSCLC)患者血清糖类抗原211(CA211)表达水平和自然杀伤(NK)细胞数与预后的相关性。方法 选取杭州师范大学附属医院2019年6月至2022年7月收治的132例NSCLC患者作为实验组,另选取同期收治的132例肺部良性病变患者作为对照组。从检验科收集数据分析NSCLC患者血清CA211表达水平和NK细胞数与患者预后关系以及影响NSCLC患者预后的相关因素。结果 实验组中性粒细胞/淋巴细胞值(NLR值)和血清CA211表达水平高于对照组(P<0.05),NK细胞数低于对照组(P<0.05);实验组血清CA211表达水平和NK细胞数呈负相关(r=-0.405,P<0.001);不同血清CA211表达水平和NK细胞数的患者淋巴结转移情况以及TNM分期存在显著性差异(P<0.05);CA211低表达者1年生存率高于CA211高表达者(P<0.05),NK细胞高水平者1年生存率高于NK细胞低水平者(P<0.05);淋巴结转移、TNM分期、CA211是影响NSCLC患者预后的危险因素(P<0.05),NK细胞是NSCLC患者预后的保护因素(P<0.05)。结论 NSCLC患者血清CA211表达水平及NK细胞数与临床病理特征及预后有密切联系。

莫诺苯宗对肺腺癌细胞自噬和凋亡的分子机制研究

目的:探究莫诺苯宗和自然杀伤细胞激活受体基因(KLRC3)对肺腺癌(LUAD)细胞凋亡和自噬的影响,为LUAD的治疗提供理论基础。方法:分别使用不同浓度莫诺苯宗处理LUAD细胞,并采用CCK-8法检测莫诺苯宗对LUAD细胞活力的影响;随后,使用80μmol/L的莫诺苯宗、50 nmol/L的KLRC3干扰质粒(si-KLRC3)、和100 nmol/L自噬抑制剂3-甲基腺嘌呤(3-MA)1.5μg/ml KLRC3过表达载体(pcDNA-KLRC3)处理细胞后采用流式细胞术和Western blotting检测细胞凋亡以及凋亡相关蛋白和自噬相关蛋白的表达量。结果:莫诺苯宗浓度大于20μmol/L时可有效减弱LUAD细胞活力,且以剂量依赖性地促进了LUAD细胞的凋亡和自噬(均P<0.05)。KLRC3在LUAD细胞中低表达,干扰KLRC3减弱了莫诺苯宗对LUAD细胞自噬和凋亡的促进作用,比较差异有统计学意义(均P<0.05)。此外,过表达KLRC3也促进了LUAD细胞的凋亡和自噬,而KLRC3和莫诺苯宗对LUAD细胞凋亡和自噬的促进作用均可被3-MA所抵消,比较差异有统计学意义(均P<0.05)。结论:莫诺苯宗可能通过促进KLRC3的表达诱导自噬进而促进LUAD细胞的凋亡。

吉林地区朝、满、汉3个民族KIR基因的分布频率研究

目的通过分析吉林地区汉族、满族及朝鲜族的杀伤细胞免疫球蛋白样受体(KIR)基因的频率与多态性,为探究KIR基因与疾病关联提供基础数据支持。方法采用聚合酶链反应-序列特异性引物(PCR-SSP)技术对吉林地区129名满族、198名朝鲜族及201名汉族人群的KIR基因进行分型。结果KIR3DL2、KIR3DL3、KIR3DP1及KIR2DL4在所有检测对象中均为100%检出。KIR2DL1、KIR2DL3、KIR2DS4、KIR3DL1及KIR2DP1等基因在这3个民族中的检出频率较高,介于93%~98%之间。相比之下,KIR2DL2、KIR2DL5、KIR3DS1、KIR2DS1、KIR2DS2、KIR2DS3及KIR2DS5的检出率较低,分布在13%~45%。特别是满族KIR2DL5(17.83%)与KIR2DS1(17.83%)的基因检出频率显著低于吉林地区朝鲜族(42.93%、47.47%)和汉族(33.83%、33.33%);吉林地区朝鲜族KIR2DL5(42.93%)与KIR2DS1(47.47%)的检出频率显著高于汉族(33.83%、33.33%)和满族(17.83%、17.83%);吉林地区汉族单体型KIRAA的频率在吉林3个受检民族中是最高的为61.19%,显著高于朝鲜族(42.93%),以上各组差异比较P<0.05,经Bonferroni校正后,Pc<0.05。结论吉林地区的朝鲜族、满族与汉族在KIR基因分布方面既体现了中国人群KIR基因多态性,又各自展示了独特的民族遗传特性和地域性。

治疗前淋巴细胞与C反应蛋白比值对结外NK/T细胞淋巴瘤预后的判断价值

目的:探讨治疗前淋巴细胞与C反应蛋白比值(LCR)对结外NK/T细胞淋巴瘤(ENKTL)预后的判断价值。方法:回顾性分析郑州大学第一附属医院收治的203例初诊为ENKTL患者的临床资料,ROC曲线得到LCR预测5 a总生存期(OS)的最佳截断值,并根据截断值将患者分为两组,绘制Kaplan-Meier生存曲线,采用Cox回归分析无进展生存期(PFS)和OS的影响因素。结果:LCR预测5 a OS的最佳截断值为0.19,低LCR组患者预后较差(P<0.001)。Cox回归分析结果表明,低LCR组ENKTL患者预后较差,PFS和OS的HR(95%CI)分别为0.462(0.336~0.636)和0.381(0.275~0.527)。结论:治疗前LCR可影响ENKTL预后,低LCR患者的预后较差。

侵袭性自然杀伤细胞白血病伴噬血细胞综合征1例

患儿,男,14岁,因反复咳嗽、咳痰1月余,加重伴发热2 d入院。入院后呼吸急促,经皮血氧饱和度明显减低,急诊胸部CT平扫示双肺大片状渗出、实变影,立即行气管插管、有创呼吸机辅助通气,积极对症治疗后,病情好转。入院第10天患儿再次发热,辅助检查示EB病毒阳性及支原体抗体IgM阳性、全血细胞减少、甘油三酯升高、纤维蛋白原降低、铁蛋白和可溶性CD25水平明显升高,确诊为噬血细胞综合征。完善骨髓穿刺可见不典型淋巴细胞,依据患儿的临床表现及流式细胞术免疫表型高度考虑侵袭性自然杀伤细胞白血病。因此,当患儿出现严重感染合并全血细胞减少,病情进展快时,应警惕噬血细胞综合征,同时需排查血液系统恶性肿瘤,及早行骨髓穿刺检查,尽早明确诊断,及时治疗。

具NK细胞的溶瘤病毒疗法的模型分析

本文建立了一类包含自然杀伤细胞(NK细胞)免疫反应的肿瘤病毒相互作用模型。首先分析了系统的边界性态,将系统的平衡点进行完整的分类,讨论了边界平衡点的局部稳定性,并从数值上验证了周期解的存在性,最后讨论了NK细胞在病毒治疗中所起到的作用。数值结果表明:a)整体肿瘤大小与病毒感染率成反比,与肿瘤生长速率成正比;b)对于NK细胞相关参数,NK细胞从淋巴结的流入速率越大,最终肿瘤越小;若产生NK细胞增殖,当增殖速率比较小时,相较于无NK增殖时,最终肿瘤变大,即较小的NK细胞增殖对治疗产生负面的影响,但当NK细胞的增殖速率过高时,将会导致肿瘤和病毒的完全清除。

自然杀伤细胞2组成员A、程序性死亡因子配体1表达检测对PD-L1阻断免疫治疗肌层浸润性膀胱癌反应性的预测价值

目的:探究自然杀伤细胞2组成员A(NKG2A)及程序性死亡因子配体1(PD-L1)表达检测对PD-L1阻断免疫治疗肌层浸润性膀胱癌反应性的预测价值。方法:选取100例肌层浸润性膀胱癌患者作为研究对象,对其行PD-L1阻断免疫治疗后,根据治疗反应性将其分为缓解组和未缓解组;对缓解组患者随访3个月,将其分为复发组和未复发组。比较两组患者NKG2A和PD-L1在CD4^(+)和CD8^(+)上的表达水平,采用ROC曲线分析NKG2A和PD-L1预测膀胱癌患者治疗反应性的价值。结果:100例研究对象中,缓解组患者72例(72.00%),未缓解组患者28例(28.00%),两组性别、年龄比较无统计学差异(均P>0.05),但缓解组患者肿瘤直径小于未缓解组,NKG2A、PD-L1/CD4^(+)和PD-L1/CD8^(+)表达水平均低于未缓解组(均P<0.05)。膀胱癌患者NKG2A、PD-L1/CD4^(+)和PD-L1/CD8^(+)表达预测免疫治疗后缓解的AUC值分别为0.771、0.724、0.710;联合诊断的AUC为0.836。72例缓解患者中,出现复发29例(40.28%),未出现复发43例(59.72%),两组性别、年龄以及肿瘤直径比较无统计学差异(均P>0.05),但复发组NKG2A、PD-L1/CD4^(+)和PD-L1/CD8^(+)表达水平均高于未复发组(均P<0.05)。NKG2A、PD-L1/CD4^(+)和PD-L1/CD8^(+)表达预测膀胱癌患者缓解后复发的AUC值分别为0.775、0.740、0.728;联合诊断的AUC为0.874。结论:NKG2A、PD-L1/CD4^(+)和PD-L1/CD8^(+)在不同治疗反应性肌层浸润性膀胱癌患者外周血中表达水平不同,三者对于膀胱癌患者PD-L1阻断免疫治疗反应性均有一定的预测价值,且三者联合预测效能最佳。

肝细胞癌过继细胞疗法研究进展

肝细胞癌是严重威胁人类生存的一类疾病,中国肝细胞癌死亡率居世界第三。由于肝细胞癌发病早期无特异性症状,晚期的治疗方案又存在复发率高等的种种弊端,因此寻找行之有效的治疗新方法迫在眉睫。过继细胞疗法是一种细胞免疫疗法,在肝脏多样化和复杂的免疫微环境中,通过结合肿瘤特异性抗原或是非特异性的调节免疫平衡,过继细胞疗法在肝细胞癌的治疗中逐渐发挥出优势。在这篇综述中我们阐述了肝细胞癌靶向治疗常用生物标志物的形态结构及信号通路,探讨总结了近年来过继细胞疗法治疗肝细胞癌的研究手段及取得的临床效果,并对接下来的研究方向进行了展望。

论超级平台扼杀式并购的反垄断法规制

超级平台扼杀式并购是平台商业模式下具有或可能具有排除、限制竞争效果的经营者集中的一种特殊情况。现行反垄断规范发端并适配于实体经济,面对超级平台扼杀式并购的规制困境可主要归结为事前申报中标准涵盖局限、实体审查中违法性判断受干扰、包容审慎原则的适用缺乏制度环境等原因。欲有效规制,需要通过适用切合平台模式的复合型指标、落实主动调查制度与标准实施评估制度,构建综合性申报体系;通过直接证据法的类型化及其分层适用、识别潜在竞争者的裁量基准的设定、限制性条件的设定,排除实体审查的障碍;通过回应性监管模式的构建及其附随的制度安排,更好地贯彻包容审慎原则。

数字平台扼杀式并购的反垄断规制困境与突破

近年来,扼杀式并购日渐演变为众多数字平台扩增市场力量,排除、限制竞争的终南捷径。这种短期内不影响市场结构的并购活动虽具有合法的交易外观,但却潜藏着深远的消极影响,其不仅会扰乱公平公正的市场竞争秩序,给企业创新带来双向阻碍,还会对消费者福利造成实质性减损。现阶段,我国数字经济领域的法律尚未与数字平台发展同频,数字平台扼杀式并购的反垄断规制仍存在一些不足。譬如,以营业额为标准的事前审查申报制度过于单薄;传统方案中数字平台相关市场界定困难;现有举证责任分配有失妥当;事后监管疲软乏力。为促使我国数字经济高质量发展,破解数字平台扼杀式并购的反垄断规制困境,可考虑将交易额纳入事前申报门槛,适度借鉴国外“守门人”制度,合理调适数字平台并购交易的举证责任,增设事后观察期制度,营造更加和谐、有序、公平、公正的数字法治生态。

复方苦参注射液联合同步放化疗治疗宫颈鳞癌术后患者的临床研究

目的:探讨宫颈鳞癌患者经根治性子宫切除术后给予复方苦参注射液联合同步放化疗方案的治疗效果。方法:选取2018年12月~2023年10月期间某院收治的80例宫颈鳞癌患者作为研究对象,根据治疗方案不同分为对照组和观察组,每组40例。两组患者均进行根治性子宫切除术,术后对照组患者给予同步放化疗方案治疗,观察组患者在对照组治疗基础上加用复方苦参注射液,两组均治疗42天。比较两组患者肿瘤标记物[鳞状上皮细胞癌相关抗原(SCC-Ag)]、炎症因子[肿瘤坏死因子-α(TNF-α)和白介素-2(IL-2)]、免疫指标[自然杀伤(NK)细胞]及不良反应发生情况。结果:治疗后,观察组患者血清SCC-Ag、TNF-α和IL-2水平均低于对照组,NK细胞水平高于对照组(P<0.05)。治疗期间,观察组患者胃肠道反应发生率低于对照组(P<0.05)。结论:复方苦参注射液联合同步放化疗治疗可抑制宫颈鳞癌术后患者肿瘤生长,降低SCC-Ag、炎症因子水平,提高NK细胞水平,且减少胃肠道不良反应的发生。

嵌合抗原受体T细胞免疫疗法在晚期胃癌中的应用进展

胃癌是最常见的恶性肿瘤之一,当前我国胃癌就诊患者仍以进展期为主,晚期患者就诊时多已失去手术治疗的机会,而传统的放疗、化疗和靶向治疗效果并不理想。嵌合抗原受体(CAR)-T细胞(CAR-T)免疫疗法作为一种新的治疗手段,在血液系统恶性肿瘤中疗效显著,也为胃癌的免疫治疗开辟了新途径。然而,由于胃癌的异质性、肿瘤微环境免疫抑制、肿瘤靶抗原逃逸及脱靶毒性等问题,使得CAR-T免疫疗法在胃癌治疗中的应用存在挑战。本文综述了CAR的结构及CAR-T治疗原理、CAR-T治疗晚期胃癌的主要靶点及治疗现状,并探讨了CAR-T治疗胃癌面临的挑战,旨在为晚期胃癌的临床免疫治疗提供新思路。

免疫细胞及相关细胞因子在骨关节炎发病及治疗中的作用

背景:骨关节炎的发生发展与免疫异常密切相关,各种免疫细胞、免疫介质在骨关节炎发病过程中的重要性不断被阐明。目的:综述免疫细胞及相关细胞因子在骨关节炎发病及治疗中的作用,为今后骨关节炎的研究和防治提供新的思路。方法:以“骨关节炎,膝,巨噬细胞,T细胞,B细胞,自然杀伤细胞,树突状细胞,细胞因子,炎症因子,免疫细胞”“osteoarthritis,knee,macrophages,T cells,B cells,natural killer cells,dendritic cells,cytokines, inflammatory factors,immune cells”为检索词在中国知网、万方、维普和PubMed和Web of Science数据库中检索已发表的相关文献,阅读标题和摘要进行初筛,在阅读全文后,最后选取98篇文献进行综述。结果与结论:(1)既往研究认为骨关节炎发病与软骨磨损相关,近年来研究认为骨关节炎是免疫细胞广泛参与的一种慢性炎性状态,随着对骨关节炎发病机制的深入研究,学者们认为骨关节炎的发病机制是由早期先天免疫反应驱动的,这种免疫反应会逐步催化退行性变,最终导致关节微环境的改变。(2)各种免疫细胞和细胞因子是影响骨关节炎修复的关键因素,其中巨噬细胞、自然杀伤细胞参与滑膜炎症反应,T细胞免疫反应参与骨关节炎软骨的降解,并加重骨关节炎的病情。(3)免疫细胞分泌的白细胞介素1β、白细胞介素6、肿瘤坏死因子α、白细胞介素17和白细胞介素37等炎性细胞因子在骨关节炎的病理生理中发挥重要作用,其中白细胞介素1β是造成关节软骨破坏最重要的炎性因子。(4)在骨关节炎病早期阶段对免疫学危险因素进行评估,能够早期有效地进行治疗,可显著降低与骨关节炎相关的残疾、发病率和成本。(5)目前干细胞及其来源外泌体、生物材料进行免疫调节治疗骨关节炎的效果已在不同的实验模型中得到证实,但将其用于临床实践之前仍有大量的实验工作要做,随着新治疗靶点的发现,针对靶点进行相关治疗将为临床骨关节炎修复带来新的希望。

肿瘤浸润性自然杀伤细胞在免疫治疗中的研究进展

自然杀伤(NK)细胞是一种具有强大细胞毒性和活性的先天淋巴细胞。基于NK细胞的免疫疗法在血液系统肿瘤的治疗中取得显著疗效,但在实体恶性肿瘤的治疗中疗效较低。该文就NK细胞的功能、表型及其肿瘤免疫治疗的研究进展作一综述。