咽环部鼻NK/T细胞淋巴瘤中EB病毒和T细胞内抗原1的表达

目的探讨咽环部鼻型NK/T细胞淋巴瘤中EB病毒的感染及其T细胞内抗原1(TIA-1)的表达和意义。方法用EBER1/2原位杂交及三步ABC法免疫组织化学染色技术,检测36例咽环部鼻NK/T细胞淋巴瘤患者EB病毒感染及T细胞内抗原1表达情况,选用的抗体有TAI-1、CD56、CD20、CD45RO,并选择10例同时期发生在鼻咽部的鼻咽癌病例做为对照。结果(1)36例病例中,男女之比为3∶1,平均年龄为44岁,以老年人为主。发病部位以鼻咽部最多。(2)36例病例的瘤细胞以大细胞、高度恶性为主,几乎所有病例临床上都有大片凝固性坏死的特点。(3)在36例病例中,EBV检出率为63.89%(23/36),T细胞内抗原1阳性表达率为91.6%(33/36)。10例鼻咽癌病例EBV检出率为80%(8/10)。结论在咽环部鼻NK/T细胞淋巴瘤中存在高水平的EB病毒隐性感染,肿瘤细胞表达TIA-1抗原可能与瘤细胞来源和其特殊的生物学行为有关。     

关于EB病毒感染与恶性淋巴瘤间关系的初步探讨

本文用免疫酶法对112例淋巴瘤患者进行血清VCA/IgA抗体效应的检测,将其结果与临床病理学资料进行综合分析,从而对淋巴瘤与EBV之间的关系作一初步探讨。研究结果表明:1.淋巴瘤患者血清VCA/IgA的抗体几何平均滴度仅次于鼻咽癌患者,在临床检验中有一定意义,2.抗体滴度与性别、年龄无密切关系。3.与组织学分型有一定关系:低度恶性的抗体滴度高,B-细胞性抗体滴度高。4.抗体滴度随着病情好转,稳定而阴转。5.本组大部分阳性病例集中在春夏多雨季节,说明EBV感染与季节,湿度有关。本文分析了112名未经治疗的淋巴瘤患者与EBV抗体效价间的关系,对这个问题做一初步探讨。     

妊娠合并滤泡性淋巴瘤1例报道并文献复习

滤泡性淋巴瘤(FL)是除弥漫大B细胞淋巴瘤(DLBCL)之外在成年人中最常见的非霍奇金淋巴瘤(NHL)之一,临床上表现为无症状性淋巴结肿大,病程进程缓慢,是一种低度恶性淋巴细胞增生性疾病。FL主要侵犯淋巴结,也可侵犯结外组织,如胃肠道、血液系统等。组织病理学是诊断FL的金标准。关于治疗方面,无化疗方案是近年来研究热点,新型靶向药物的开展和研究的不断深入,为FL患者的治疗带来新的希望。不同患者临床异质性明显,预后差异较大。本文回顾分析1例妊娠期间意外发现的FL患者,并复习相关文献,提高临床医生对该病的认识,真正使患者得到有效诊治。     

EB病毒DNA、LDH、铁蛋白联合检测在诊断弥漫性大B细胞淋巴瘤中的意义

目的 观察分析EB病毒DNA、LDH、铁蛋白联合检测在诊断弥漫性大B细胞淋巴瘤中的意义。方法选取2020年12月—2022年12月本院收治的淋巴瘤患者50例和淋巴结炎患者50例为研究对象,分为淋巴瘤组与对照组。对两组进行EB病毒DNA、LDH、铁蛋白联合检测,测定血液中EB病毒DNA的阳性检出率、LDH水平和铁蛋白水平的区别。结果 淋巴瘤组DNA的阳性检出率要明显高于对照组,差异有统计学意义（P<0.05）;血清的对比中淋巴瘤组中的LDH和铁蛋白要明显高于对照组,LDH和铁蛋白高代表确诊恶性肿瘤的概率就越大,差异有统计学意义（P<0.05）。结论 EB病毒DNA、LDH、铁蛋白联合检测对诊断弥漫性大B细胞淋巴瘤具有重大意义,检测效果非常显著。     

血管免疫母细胞性T细胞淋巴瘤引发急性肾衰竭1例

患者,男,66岁,因“发现血肌酐升高半年余。”于2019-04-13入院。患者半年余前无明显诱因下出现咳嗽、气急至外院呼吸科就诊时发现血肌酐升高,当时血肌酐170.2μmol/L,白蛋白26.3g/L,球蛋白55.7g/L,血红蛋白95g/L,免疫球蛋白G 42.3g/L,尿检结果未见,查肺部CT:两肺间质性肺炎考虑,考虑:特发性肺间质纤维化,予“吡非尼酮400mg每日两次”治疗,气急有好转。2月前患者咳嗽加重,至我院呼吸科就诊,查血肌酐408μmol/L,无明显尿量减少,未服用中草药、止痛药等,遂至我科就诊,门诊拟“肾功能不全”收住入院。既往有糖尿病1年余,予诺和锐30R 14单位每日一次治疗,血糖控制一般。     

HIV相关淋巴瘤诊治进展

[摘要]　HIV相关淋巴瘤是常见的HIV相关肿瘤之一,在联合抗反转录病毒治疗（combination antiretroviral therapy, cART）出现之前,其治疗效果极差。在cART时代,HIV相关淋巴瘤的基础及临床研究取得了重大进展,这些为挖掘治疗新靶点提供了依据,使优化HIV相关淋巴瘤的诊治成为可能。本文对近年来HIV相关淋巴瘤的诊断和治疗进展进行综述。     

弥漫性大B细胞淋巴瘤的研究进展

弥漫性大B细胞淋巴瘤为非霍奇金淋巴瘤的一种常见类型,约占非霍奇金淋巴瘤所有病例的1/3,具有较高的发病率.此类淋巴瘤可由原发结外病变或原发淋巴结起病,＞50％患者就诊时存在结外病变侵犯,而最为常见的结外病变有骨髓、胃肠道等.弥漫性大B细胞淋巴瘤为高度一致性肿瘤,不同亚型患者存在不同临床表现、生物学特性、治疗反应等,且预...     

巨细胞病毒感染与糖尿病发病机制研究进展

巨细胞病毒（cytomegalovirus,CMV）属于β 疱疹病毒亚科的双链DNA病毒,人类普遍易感,世界范围内CMV感染率为40%～90%［1］,是引起先天和围产期感染,导致新生儿先天畸形［2］、智力低下、发育迟缓等后遗症的最常见病原体。在免疫功能低下人群,如人类免疫缺陷病毒（HIV）感染和接受器官移植的患者中,CMV感染发病率很高,可导致视网膜炎、肺炎、胃肠炎等疾病,是该患者人群的主要致死性并发症之一。在免疫正常的个体中,主要引起无症状感染,并且持续潜伏在机体中。本文对CMV感染导致糖尿病的发病机制予以综述。     

乙型肝炎病毒感染对B细胞性非霍奇金淋巴瘤预后的影响

目的探讨乙型肝炎病毒感染对B细胞性非霍奇金淋巴瘤预后的影响。方法应用ELISA法测定B细胞性非霍奇金淋巴瘤患者确诊时的乙型肝炎病毒抗原抗体两对半。结果28例B细胞性非霍奇金淋巴瘤患者中,伴乙型肝炎病毒感染者12例（占43％）,表面抗原阳性者4例（占14％）;伴乙型肝炎病毒感染的B细胞性非霍奇金淋巴瘤患者的化疗后完全缓解率低于无乙型肝炎病毒感染的B细胞性非霍奇金淋巴瘤患者。结论携带乙型肝炎病毒的B细胞非霍奇金淋巴瘤患者化疗后肝功能损害的发生率高,且与乙型肝炎病毒阴性组对比,患者预后不佳。     

COX联合XGBoost的原发睾丸弥漫大B细胞淋巴瘤预后模型构建与验证

目的 原发睾丸弥漫大B细胞淋巴瘤全球发病率逐年增长,且因为血睾屏障的存在,死亡率高,目前尚缺乏多中心的大型回顾性分析数据进行疾病的预后研究。方法 从SEER数据库的22个中心机构获取2000—2019年期间,诊断为原发睾丸弥漫大B细胞淋巴瘤的患者资料进行回顾性分析,共纳入816例患者,按7:3的比例随机分为建模组和验证组。采用多变量COX逐步回归联合XGBoost机器学习模型筛选预后特征变量,将二者筛选出的共同预后因子构建列线图并对其重要度进行排序;时间依赖性ROC曲线验证模型的预测性能,校准曲线确定模型的一致性,决策曲线(decision curve analysis,DCA)评估模型的临床实用性与有效性。结果 COX回归结合XGBoost筛选出的共同预后因子为：年龄、手术、放疗、双侧发病、化疗、系统治疗、Ann Arbor分期;将其按照重要度排序,由大到小依次为：年龄、系统治疗、Ann Arbor分期、手术、双侧发病、化疗、放疗。基于联合模型筛选出的共同预后因子构建列线图,ROC曲线、校准曲线和DCA曲线显示模型具有良好的预测性能和临床实用性。结论 本研究构建的机器学习模型结合回归...     

经典型霍奇金淋巴瘤EB病毒感染和p16蛋白表达的相关性研究

目的探讨EB病毒在经典型霍奇金淋巴瘤（CHL）中的感染和p16蛋白表达的关系。方法应用EBER-1寡核苷酸探针以原位杂交方法检测80例CHL组织中的EBV编码的小RNA;用免疫组化方法检测p16蛋白表达。结果80例CHL患者中,男52例,女28例,男女之比为1．86：1,其中52例CHL男性患者中,EBER-1阳性率63．46％;28例CHL女性患者中,EBER-1阳性率39．29％,两者比较具有统计学意义（Х^2=4．298,P=0．038）。儿童和老年人中CHL患者共45例,其EBV表达阳性率75．56％,多于成年人的28．57％,两者比较差异具有统计学意义（Х^2=20．13,P=0．000）。EBER．1阳性表达定位在R—s细胞核上,其阳性表达率为55．00％,各亚型CHL的EBV潜伏感染检出率分别是：混合细胞型（MC）71．79％,淋巴消减型（LD）42．85％,淋巴细胞为主型（LP）47．06％,结节硬化型（NS）29．41％,且MC型明显高于NS型（Х^2=8．787,P=0．003）;p16蛋白阳性表达定位在R—S细胞的细胞核和细胞浆,其总的阳性表达率为45％,各亚型阳性率分别为：IJP47．05％,MC48．71％,NS35．29％,LD42．85％;p16蛋白与EBER-1之间呈负相关（r=-0．242,P〈0．05）。结论CHL发生可能与EBV感染有关,且p16蛋白的高表达为协助诊断CHL提供了依据。     

以树突细胞为基础的抗乙型肝炎病毒免疫治疗现状与展望

DC是强大的APC,制备HBV抗原特异性DC疫苗,诱生抗原特异性CTL,可以有效控制HBV感染;DC还可分泌Exosome,后者作为新型非细胞结构性疫苗,有望成为抗HBV免疫治疗的生力军。     

儿童传染性单核细胞增多症T细胞亚群及B细胞的动态变化研究

目的探讨儿童传染性单核细胞增多症（infectiousmononucleosis,IM）不同时期外周血T细胞亚群CD3＋,CD4＋CD8＋细胞及B细胞CD15＋,CD19＋和CD23＋的改变及其变化规律。方法选择2006年3月至2008年3月四川省人民医院儿科收治的30例传染性单核细胞增多症患儿为研究对象（研究组,n=30）,选择同期入托体检,无过敏性疾病史及无阳性过敏疾病家族史的健康儿童纳入对照组（n=25）（本研究遵循的程序符合四川省人民医院人体试验委员会制定的伦理学标准,得到该委员会批准,分组征得受试对象监护人的知情同意,并与其签署临床研究知情同意书）。两组儿童性别、年龄比较,差异无显著意义（P〉0．05）。研究组分别在传染性单核细胞增多症急性期,病程1个月、3个月、6个月时,采集静脉血2mL,对照组采血方式与研究组相同,采用肝素抗凝、流式细胞术方法分别检测其外周血淋巴细胞CD3＋,CD4＋,CD8＋和CD15＋及CD19＋CD25＋表达率,并进行比较。结果①研究组急性期CD4＋为（14．84±5．03）％,CD4＋／CD8＋为（0．25±0．13）％,CD19＋为（3．89±1．32）％及CD19＋CD23＋为（0．24±0．13）％,较对照组明显降低;CD3＋为（82．55±5．49）％,CD8＋为（66．17±8．10）％,较对照组明显增高,与其余各组比较,差异有显著意义（P〈0．001）;②研究组内随时间推移及感染的控制,CD4＋,CD4＋／CD8＋,CD19＋及CD19＋CD23＋逐渐升高,CD3＋,CD8＋细胞逐渐降低;③研究组病程6个月时,CD3＋为（67．98±8．01）％、CD4＋为（32．81±6．79）％、CD8＋为（33．96±7．37）％、CD4＋／CD8＋为（0．93±0．31）％及CD19＋CD23＋为（1．30±0．50）％,与对照组比较,差异无显著意义（P〉0．05）,但病程6个月时,CD9＋为（14．60±4．80）%,与对照组比较,差异有显著意义（P〈0．001）。结论单核细胞增多症急性期CD3＋,CD8＋明显增高,CD4＋,CD4＋／CD8＋,CD19＋及CD19＋,CD23＋。明显降低,病程6个月时,CD3＋,CD4＋,CD8＋,CD4＋／CD8＋及CD19＋CD23＋表达正常,但CD19＋仍低于正常水平。这提示,单核细胞增多症患儿存在继发性免疫功能低下,并持续至临床症状消失后较长时间,应引起重视。该结果可为临床应用静脉丙种球蛋白治疗单核细胞增多症提供一定理论依据。     

克拉屈滨联合阿糖胞苷治疗高危/难治性儿童急性髓细胞白血病及侵袭性NK/T细胞淋巴瘤

目的探讨应用克拉屈滨联合阿糖胞苷治疗高危/难治性儿童急性髓细胞白血病(AML)及侵袭性NK/T细胞淋巴瘤(NKTCL)的有效性及安全性。 方法选择2015年12月至2017年7月,于首都儿科研究所附属儿童医院血液科治疗的2例高危/难治性AML患儿及1例侵袭性NKTCL患儿为研究对象。对于高危/难治性AML患儿,采用克拉屈滨＋阿糖胞苷＋米托蒽醌＋重组人粒细胞集落刺激因子(CLAG-M)方案治疗,即d 2～6静脉滴注克拉屈滨5 mg/(m²·d),d 2～6静脉滴注阿糖胞苷2 g/(m²·d),d 2～4静脉滴注米托蒽醌10 mg/(m²·d),d 1～6皮下注射重组人粒细胞集落刺激因子3～5 μg/(kg·d)。对于侵袭性NKTCL患儿,采用克拉屈滨＋阿糖胞苷方案治疗,即d 1～5静脉滴注克拉屈滨5 mg/(m²·d),d 1～5静脉滴注阿糖胞苷500 mg/(m²·d) 。回顾性分析3例患儿的临床病例资料,对其临床表现、诊断、治疗及预后进行总结。本研究符合2013年修订的《世界医学协会赫尔辛基宣言》的要求,征得受试儿监护人知情同意,并于治疗前与其签署临床治疗知情同意书。 结果①患儿1为女性,16岁,临床诊断为高危/难治性AML M5。患儿1接受CLAG-M方案诱导治疗1个疗程后,达到完全缓解,骨髓细胞形态学检查未见白血病细胞,流式细胞术检测结果显示,骨髓微小残留病变(MRD)为1.37%,MLL-AF9融合基因定量检测结果为0。但是,该例患儿在后续巩固治疗中,因骨髓抑制(血小板减少)导致的颅内出血而死亡。②患儿2为女性,6岁,临床诊断为高危/难治性AML M2。患儿2接受CLAG-M方案诱导治疗1个疗程后,达到完全缓解,骨髓细胞形态学检查未见白血病细胞,流式细胞术检测结果显示,骨髓MRD为0.81%;接受CLAG-M方案治疗第2个疗程后,骨髓MRD<0.001%。随后,患儿2接受单倍体异基因造血干细胞移植,迄今移植后无事件生存时间已达2年。③患儿3为男性,4岁,因"皮肤破损5月余"在本院接受住院治疗,临床诊断为侵袭性NKTCL。患儿3接受克拉屈滨＋阿糖胞苷治疗1个疗程7 d后,未再出现新皮疹;20 d后,皮肤出血、溃烂明显减轻,鼻翼、躯干及四肢破损皮肤约80%结痂,鼻翼处皮肤破损范围约缩小50%;40 d后,50%～60%躯干、四肢破损皮肤愈合,达到部分缓解。患儿3最终带瘤进行同胞全相合造血干细胞移植后1个月,骨髓细胞形态学复查结果为完全缓解,骨髓MRD<0.001%。移植后2个月,患儿3侵袭性NKTCL复发,对其进行供者淋巴细胞输注治疗1次,肿瘤负荷未再增多。迄今,患儿3移植后带瘤生存时间已达1年。④3例患儿在治疗过程中,均出现Ⅳ度骨髓抑制及不同程度感染,经对症及抗感染治疗后,上述症状均被控制。 结论CLAG-M方案、克拉屈滨＋阿糖胞苷方案治疗部分高危/难治性儿童AML及侵袭性NKTCL有效,是此类患儿进行造血干细胞移植前的有效桥接手段。防治感染是这2种方案治疗高危/难治性AML及侵袭性NKTCL患儿成败的关键。由于本研究仅为回顾性病例研究,应用克拉屈滨联合阿糖胞苷治疗高危/难治性儿童AML及侵袭性NKTCL的疗效,仍有待大样本量的多中心、随机对照研究进一步证实。     

肝包虫病合并HBV感染患者Th17、CD4+细胞表面PD-1/PD-L1的表达水平及意义

目的探讨肝包虫合并乙型肝炎病毒(HBV)感染患者辅助性T细胞17(Th17)、CD4⁺细胞表面程序性死亡分子-1/程序性死亡分子1配体(PD-1/PD-L1)的表达水平及其临床意义。方法选取2014年9月一2019年9月新疆医科大学第一附属医院收治的肝包虫病患者作为研究对象﹐其中100例肝包虫病合并HBV感染患者为合并HBV感染组,肝包虫病无HBV感染患者88例为非HBV感染组﹐采用流式细胞仪检测外周血Th17,CD4⁺细胞表面PD-1,PD-L1表达水平。结果合并HBV感染组患者乙型肝炎家族史,B~C Child分级占比均高于非HBV感染组(P<0.05);肝功能指标[谷丙转氨酶(ALT)、谷草转氨酶(AST),γ-谷氨酰转肽酶(γ-GT)]水平以及Th17 PD-1、Th17 PD-L1,CD,PD-1,CD4⁺PD-L1表达水平均高于非HBV感染组(P<0.05);Child分级A级肝包虫病患者的Th17 PD-1,Th17 PD-L1,CD4⁺PD-1,CD4⁺PD-L1表达水平均低于Child分级B~C级患者(P<0.05)。结论HBV感染会影响肝包虫病患者的肝功能及外周血Th17,CD4⁺细胞表面PD-1,PD-L1表达水平,肝功能严重程度可能与外周血Th17,CD4⁺细胞PD-1,PD-L1表达存在关系。     

Tumor-specific peptide-based vaccines containing the conformationally biased, response-selective C5a agonists EP54 and EP67 protect against aggressive large B cell lymphoma in a syngeneic murine model

Vaccines to large B cell lymphoma were made by the covalent attachment of an epitope from the gp70 glycoprotein (SSWDFITV) to the N-termini of the conformationally biased, response-selective C5a agonists EP54 (YSFKPMPLaR) and EP67 (YSFKDMP(MeL)aR). Syngeneic Balb/c mice were immunized with these EP54/EP67-containing vaccines and challenged with a lethal dose of the highly liver metastatic and gp70-expressing lymphoma cell line RAW117-H10 to evaluate the ability of these vaccines to induce protective immune outcomes. All mice immunized with SSWDFITVRRYSFKPMPLaR (Vaccine 2) and SSWDFITVRRYSFKDMP(MeL)aR (Vaccine 3) were protected to a lethal challenge of RAW117-H10 lymphoma (>170 days survival) and exhibited no lymphoma infiltration or solid tumor nodules in the liver relative to unvaccinated controls (<18 days survival). Vaccines 2 and 3 contained the protease-sensitive double-Arg (RR) linker sequence between the epitope and the EP54/EP67 moieties in order to provide a site for intracellular proteases to separate the epitope from the EP54/EP67 moieties once internalized by the APC and, consequently, enhance epitope presentation in the context of MHC I/II. These protected mice exhibited an immune outcome consistent with increased involvement of CD8⁺ and/or CD4⁺ T lymphocytes relative to controls and mice that did not survive or showed low survival rates as with Vaccines 1 and 4, which lacked the RR linker sequence. CD8⁺ T lymphocytes activated in response to Vaccines 2 and 3 express cytotoxic specificity for gp70-expressing RAW117-H10 lymphoma cells, but not antigen-irrelevant MDA-MB231A human breast cancer cells. Results are discussed against the backdrop of the ability of EP54/EP67 to selectively target antigens to and activate C5a receptor-bearing antigen presenting cells and the prospects of using such vaccines therapeutically against lymphoma and other cancers.     

Tim-3 alters the balance of IL-12/IL-23 and drives TH17 cells: Role in hepatitis B vaccine failure during hepatitis C infection

Hepatitis B virus (HBV) vaccination is recommended for individuals with hepatitis C virus (HCV) infection given their shared risk factors and increased liver-related morbidity and mortality upon super-infection. Vaccine responses in this setting are often blunted, with poor response rates to HBV vaccinations in chronically HCV-infected individuals compared to healthy subjects. In this study, we investigated the role of T cell immunoglobulin mucin domain-3 (Tim-3)-mediated immune regulation in HBV vaccine responses during HCV infection. We found that Tim-3, a marker for T cell exhaustion, was over-expressed on monocytes, leading to a differential regulation of IL-12/IL-23 production which in turn T_H17 cell accumulation, in HCV-infected HBV vaccine non-responders compared to HCV-infected HBV vaccine responders or healthy subjects (HS). Importantly, ex vivo blockade of Tim-3 signaling corrected the imbalance of IL-12/IL-23 as well as the IL-17 bias observed in HBV vaccine non-responders during HCV infection. These results suggest that Tim-3-mediated dysregulation of innate to adaptive immune responses is involved in HBV vaccine failure in individuals with chronic HCV infection, raising the possibility that blocking this negative signaling pathway might improve the success rate of HBV immunization in the setting of chronic viral infection.     

Genetic polymorphisms of CXCR5 and CXCL13 are associated with non-responsiveness to the hepatitis B vaccine

A cohort based study has been undertaken to investigate the possible association of genetic polymorphisms in genes functionally related to follicular T helper (TfH) cells with non-responsiveness to hepatitis B virus (HBV) vaccination. A total of 24 single nucleotide polymorphisms (SNPs) in 6 TfH related genes (CXCR5, ICOS, CXCL13, IL-21, BCL6 and CD40L) were investigated in 20 non-responders and 45 responders to HBV vaccination. Genetic association analysis revealed that three SNPs (rs497916, rs3922, rs676925) in CXCR5 and one SNP (rs355687) in CXCL13 were associated with hepatitis B vaccine efficacy. In addition, significantly unbalanced distributions of two haplotypes, defined by three SNPs (rs497916, rs3922, rs676925) within CXCR5, were also seen between non-responders and responders. Furthermore, we demonstrated that the rs3922 “GG” genotype was associated with higher levels of CXCR5 than the “AG” and “AA” genotype in a group of healthy volunteers. A dual luciferase report assay was used to confirm that the “G” allele in rs3922 may lead to higher gene expression than the “A” allele, implicating that rs3922 might be a functional SNP affecting CXCR5 expression. These results indicated that polymorphism associated changes in CXCR5 expression in TfH cells may be associated with non-responsiveness to hepatitis B vaccination.     

Monitoring the efficacy of infant hepatitis B vaccination and revaccination in 0- to 8-year-old children: Protective anti-HBs levels and cellular immune responses

Vaccination against hepatitis B virus (HBV) is recommended worldwide. The aim of this study was to assess the efficacy of infant hepatitis B vaccination and revaccination in 0- to 8-year-old children in the context of protective anti-HBs levels and cellular immune responses. Using a random questionnaire survey, 1695 pre-school children were recruited as research subjects during January 2015 to June 2017. Blood samples were obtained to measure HBV serological markers as well as peripheral immunocytes. The children were divided into non-, low- and hyper- responsive groups (NR, LR, and HR) based on the vaccination efficacy. Additionally, the effect of revaccination on the NR group was evaluated at 1 month after completion of the vaccination course. Among a total of 1695 children, 1591 (93.86%) were infants who were followed while undergoing their primary course of hepatitis B vaccination at the 0-1-6 month schedule, and 1249 (79.30%) of them developed antibodies against HBsAg (anti-HBs) titers greater than 10 IU/L. The results of immunocyte studies indicated that the CD8⁺ T cells, CD4⁺CD45RO⁺ T cells, CD8⁺CD45RA⁺ T cells, and T follicular helper (Tfh) cells increased significantly in NR compared with HR. However, lymphocytes, CD4⁺ T cells, and CD4⁺CD45RA⁺ T cells in NR were lower than that in HR. 96 of the non-response cases showed seroprotection after revaccination among 103 cases. Therefore, most of the preschool children who received hepatitis B vaccine in infancy achieved significant seroprotection. Seroconversion rates of individuals revaccinated after initial vaccination failure were significantly higher than those after primary vaccination. Different vaccination efficacy groups showed significant changes in circulating immunocytes, which might be a factor affecting the recombinant HBV vaccine’s immune effectiveness.