哮喘患儿T细胞亚群及细胞因子的变化

哮喘发病机理方面的研究已成为当今哮喘的研究热点。目前认为Ｔ细胞的激活及其释放的细胞因子在哮喘的发病中起着重要作用。关于哮喘患者的Ｔ细胞亚群改变 ,各家报道结果不一。现将我们观察的结果报告如下。对象1998年 1月～ 1999年 1月间在我院诊断为支气管哮喘的患儿 38例 ,均符合全国儿科哮喘协作组制定的哮喘诊断标准[1] 。发作期 38例 ,其中男 2 9例 ,女 9例 ;平均年龄 (8±4)岁 (2～ 14岁 )。其中有 2 7例缓解期时第 2次采血 ,距第 1次采血时间间隔为 (2 0± 3)ｄ。对照组 2 0例 ,均为我院同期门诊体检正常儿童 ,其中男 14例 ,女 6例 …     

新生儿窒息外周血T细胞亚群及SIL—2R变化

为探讨新生儿窒息与免疫的关系，我们对２５例窒息新生儿测定了外周血Ｔ细胞亚群，１７例测定了血清可溶性白细胞介素－２受体（ＳＩＬ－２Ｒ）。结果新生儿窒息后ＣＤ４＾＋细胞减少（Ｐ〈０．０１）、ＣＤ８＾＋细胞增加（Ｐ〈０．０１），ＣＤ４／ＣＤ８比值降低（Ｐ〈０．００２５）。而且，重度窒息患儿ＣＤ３＾＋细胞亦明显减少（Ｐ〈０．０５）；血清ＳＩＬ－２Ｒ水平显著升高。提示窒息缺氧可导致新生儿免疫功能下降，复苏后     

新生儿HIE外周血T细胞亚群、IL-6、IL-8水平变化及临床意义探讨

目的观察新生儿HIE外周血T细胞亚群、IL-6、IL-8水平变化,并探讨其临床意义.方法收集50例HIE患儿和30例正常新生儿外周血,采用双色免疫荧光标记法及流式细胞仪检测CD3+、CD4+、CD8+T细胞免疫表型,采用酶标免疫吸附法检测IL-6、IL-8.记录HIE患儿临床资料.结果HIE组外周血CD3+、CD4+、CD8+细胞水平低于对照组.IL-6、IL-8高于对照组,差异有高度显著性(P＜0.01);不同病情、不同转归HIE组CD3+、CD4+、CD8+、IL-6差异有高度显著性(P＜0.01),即CD3+、CD4+、CD8+降低、IL-6升高越显著者,病情越重,预后越差.结论新生儿HIE免疫功能受损.CD3+、CD4+、CD8+细胞和IL-6、IL-8水平对临床早期判断病情严重性、估计预后、指导治疗有一定意义.     

支气管哮喘患儿可溶性白细胞介素2受体和T细胞亚群变化

本文采用MCAb间接免疫荧光法和双抗体夹心ELISA法，测定哮喘患儿外周血T细胞亚群和可溶性白细胞介素2受体（sIL-2R）水平变化，结果哮喘发作组CD、CD4／CD8、sIL-2R均显著高于对照组（P均＜0．of）和缓解组（P唯有CD4＜O．05，余均＜O．01），而缓解组与对照组比均无差异（P均＞0．05），发作组CD8明显低于对照组和缓解组（P均＜0.01）。T细胞亚群和sIL-2R可做为哮喘不同时期观察病情和预防发作的指标。     

病毒性肝炎T细胞亚群和几种细胞因子变化的研究

为了探讨小儿病毒性肝炎发病的细胞免疫机制，应用不标记抗体桥联酶标技术（ＡＰＡＡＰ法）检测了５６例病毒性肝炎患儿的外周血Ｔ细胞亚群及膜性白细胞介素２受体（ｍＩＬ－２Ｒ）表达率。应用酶联免疫吸附（ＥＬＩＳＡ）法分别检测了４９例病毒性肝炎患儿单个核细胞培养上清液（ＰＢＭＣｓ）中肿瘤坏死因子α（ＴＮＦα）、白细胞介素６和８（ＩＬ－６、ＩＬ－８）及α干扰素（ＩＦＮ－α）浓度。结果显示：甲型肝炎（简称甲肝）急性期、慢性乙型肝炎（简称乙肝）及丙型肝炎（简称丙肝）组与正常对照比较，ＣＤ４细胞降低，ＣＤ８细胞升高。用植物血凝素（ＰＨＡ）刺激前，甲肝急性期患儿ｍＩＬ－２Ｒ表达率明显高于其他各组，用ＰＨＡ刺激后，各组ｍＩＬ－２Ｒ表达率均显著高于刺激前，但乙肝及丙肝组ｍＩＬ－２Ｒ表达率与正常对照比较则明显降低。甲肝急性期、乙肝及丙肝患儿ＰＢＭＣｓＴＮＦα、ＩＬ－６、ＩＬ－８均较正常对照组升高，而α干扰素（ＩＦＮ－α）均较正常对照组降低。甲肝恢复期ＣＤ４、ＣＤ８和ＰＨＡ刺激前ＰＢＭＣ上ｍＩＬ－２Ｒ表达率以及上述各细胞因子水平均恢复正常。提示细胞免疫功能紊乱与小儿病毒性肝炎的发病及肝损害过程有关。     

新生儿窒息外周血T细胞亚群及SIL—2R变化

为探讨新生儿窒息与免疫的关系，我们对25例窒息新生儿测定了外周血T细胞亚群，17例测定了血清可溶性白细胞介素-2受体（SIL-2R）。结果新生儿窒息后CD4+细胞减少（P＜0．01）、CD8+细胞增加（P＜0．01），CD4／CD8比值降低（P＜0．0025）。而且，重度窒息患儿CD细胞亦明显减少（P＜0．05）。血清SIL—2R水平显著升高。提示窒息缺氧可导致新生儿免疫功能下降，复苏后上述指标可恢复正常，并对其发生机理及临床意义进行了讨论。     

新生儿HIE外周血T细胞亚群、IL—6、IL—8水平变化及临床意义探讨

目的:观察新生儿HIE外周血T细胞亚群、IL-6、IL-8水平变化,并探讨其临床意义。方法:收集50例HIE患儿和30例正常新生儿外周血,采用双色免疫荧光标记法及流式细胞仪检测CD3+、CD4+、CD8+T细胞免疫表型,采用酶标免疫吸附法检测IL-6、IL-8。记录HIE患儿临床资料。结果:HIE组外周血CD3+、CD4+、CD8+细胞水平低于对照组,IL-6、IL-8高于对照组,差异有高度显著性（P<0.01）;不同病情、不同转归HIE组CD3+、CN4+、CD8+、IL-6差异有高度显著性（P<0.01）,即CD3+、CD4+、CD8+降低、IL-6升高越显著者,病情越重,预后越差。结论:新生儿HIE免疫功能受损,CD3+、CD4+、CD8+细胞和IL-6、IL-8水平对临床早期判断病情严重性、估计预后、指导治疗有一定意义。     

注意缺陷多动障碍患儿T淋巴细胞亚群及细胞因子的初步研究

目的测定注意缺陷多动障碍(ADHD)患儿T淋巴细胞亚群和白细胞介素-1β(IL-1β)、6(IL-6)、肿瘤坏死因子-α(TNF-α)水平,探讨ADHD与免疫的关系.方法ADHD组30例7～13岁符合DSM-ⅣADHD诊断标准的男性儿童;对照组22例同龄的正常健康男性儿童,收集外周血测定T淋巴细胞亚群及细胞因子水平.结果ADHD组CD3+和CD8+细胞数较对照组降低;ADHD组血清IL-1β水平高于对照组,而TNF-α低于对照组;TNF-α水平与儿童行为量表(CBCL)中注意问题、外向性行为问题及划销测验失误率呈负相关,IL-1β与划销测验失误率呈正相关.结论ADHD存在着Ts细胞功能的低下;ADHDIL-1β的增高和TNF-α的降低可能与ADHD的神经发育异常有关;TNF可能作为ADHD遗传的一个候选基因;TNF-α降低可能是ADHD的外向性行为问题的状态标记.     

支原体肺炎患儿辅助性T淋巴细胞亚群TH1、TH2细胞状况

目的　探讨肺炎支原体肺炎急性期患儿外周血淋巴细胞亚群以及辅助性T淋巴细胞亚群TH1、TH2细胞的改变 ,为免疫治疗的可能性提供依据。方法　采用流式细胞仪技术 (FACS)检测了3 5例支原体肺炎急性期患儿外周血T淋巴细胞亚群以及NK细胞和B细胞 ,同时通过检测分泌细胞因子γ干扰素 (IFN γ)、白细胞介素 4(IL 4)的CD+ 4细胞方法 ,测出相应TH1、TH2细胞的百分比 ,并与2 8例正常儿童进行比较。同时对 3 5例支原体肺炎患儿中的 3 0例进行了血清免疫球蛋白及精制结核菌素 (PPD)皮肤试验。全部患儿均系在我院住院的患儿 ,男 15例 ,女 2 0例 ,年龄 3～ 13岁 ,平均 9岁。对照组男 14例 ,女 14例 ,年龄 3～ 12岁 ,平均 7岁。结果　支原体肺炎患儿急性期外周血CD+ 3 、CD+ 4T细胞百分率为 68 0 0± 6 66及 3 7 86± 5 84,较对照组 63 71± 7 92及 3 4 54± 6 2 3高 ,(P <0 0 5) ;患儿外周血TH1细胞百分率为 14 13± 8 46,对照组为 2 0 77± 6 89,两者差异有非常显著意义 (P =0 0 0 1)。NK细胞及TH1/TH2比值在患儿组降低 (P分别为 <0 0 1和 <0 0 5)。两组间CD8、TH2、B细胞百分率及CD4/CD8比值差异无显著意义。 3 0例患儿之血清免疫球蛋白与同龄正常儿童比较 ,IgG全部正常 ;IgA升高 7例 ;IgM升高 4例。皮肤P     

支气管哮喘患儿T淋巴细胞及细胞因子的变化

为观察儿童支气管哮喘时Ｔ淋巴细胞亚群分布以及Ｔ细胞活化相关因子及受体的表达状况，应用放射免疫分析等技术，对３４例发作期、２５例缓解期支气管哮喘患儿和１５例正常对照的外周血Ｔ淋巴细胞亚群、血浆及淋巴细胞膜表面白细胞介素－２受体（ＩＬ－２Ｒ）和相关细胞因子等水平进行系统检测。结果：（１）发作期患儿外周血Ｔ细胞亚群ＣＤ３，ＣＤ４及ＣＤ４／ＣＤ８值与缓解期患儿及正常对照比较差异无显著意义，但发作期ＣＤ８高于正常对照（Ｐ＜０．０１）和缓解组（Ｐ＜０．０１）；（２）发作期患儿血浆可溶性ＩＬ－２Ｒ、（ｓＩＬ－２Ｒ）、ＩｇＥ水平明显高于缓解期患儿和正常对照（Ｐ＜０．０１）；（３）免疫电镜观察显示，发作期患儿淋巴细胞膜表面ＩＬ－２Ｒ表达高于正常对照（Ｐ＜０．０５）。提示：（１）哮喘患儿外周Ｔ淋巴细胞亚群的分布发生了变化，哮喘发作期Ｔ淋巴细胞处于激活状态；（２）血浆ｓＩＬ－２Ｒ、ＩｇＥ水平与哮喘病情变化密切相关，可作为临床哮喘病情监测的指标。     

难治性肺炎支原体肺炎患儿肺泡灌洗液中白细胞介素-6、白细胞介素-10及T细胞亚群水平研究

目的 探讨难治性肺炎支原体肺炎患儿肺泡灌洗液(BALF)中白细胞介素(IL)-6、IL-10及T细胞亚群水平变化.方法 选取确诊为难治性肺炎支原体肺炎患儿53例作为观察组,选取同期就诊于我院的支气管异物患儿30例作为对照组.采用双抗体夹心ABC-ELISA法检测BALF中IL-6、IL-10水平及采用流式细胞仪检测T细胞免疫表型CD3+、CD4+和CD8+水平.结果 观察组患儿BALF中IL-6、IL-10水平分别为(63.25±18.61) ng/ml、(31.83±8.33) ng/ml,明显高于对照组的(30.51 ±1.34) ng/ml、(11.01 ±2.91) ng/ml,两组比较差异有统计学意义(P＜0.05);观察组患儿BALF中T细胞亚群CD3+、CD4+、CD8+、CD4 +/CD8+分别为(48.47±2.88)％、(21.16±6.29)％、(23.04±4.63)％、0.94±0.33,明显低于对照组的(64.24±3.06)％、(34.34±7.59)％、(26.71±5.29)％、1.56±0.67,两组比较差异有统计学意义(P＜0.05).结论 难治性肺炎支原体肺炎患儿BALF中IL-6、IL-10水平明显增高及T细胞免疫功能紊乱,提示细胞免疫在难治性肺炎支原体肺炎的发病中起重要作用.     

Long-term study on T lymphocyte subsets in newly diagnosed type 1 diabetes mellitus

T lymphocyte subsets in peripheral blood from 16 newly diagnosed type 1 diabetic children were studied prospectively at four time intervals: as soon as possible after diagnosis and 1, 4 and 12 months later. T lymphocyte subsets were analysed using monoclonal antibodies and counted by cytofluorimetry. The percentage of T lymphocytes (OKT₃⁺ cells) did not change at the four study times. The percentage of helper/inducer T cells (OKT₄⁺ cells) was high at the diagnosis (43.1 ± 2.1%), but decreased after 1 and 4 months with no difference in the control values. The percentage of suppressor/cytotoxic T lymphocytes (OKT₈⁺ cells) was low at the diagnosis, but increased after 1 and 4 months. The OKT₄/OKT₈ ratio was 2.31 ± 0.22 at the diagnosis study, decreasing to 1.83 after 1 month, compared with 16 sex- and age-matched control children. The high percentage of helper/inducer T lymphocytes and low number of suppressor/cytotoxic T cells at onset of diabetes favour immune reactions that lead to β-cell damage.     

匹多莫德对哮喘患儿IL-16及免疫功能的影响

目的 探讨白介素-16(IL-16)在儿童哮喘中的发病机制,观察匹多莫德在儿童哮喘防治中的疗效.方法 将90例哮喘患儿随机分为治疗组55例,对照组35例;对照组予哮喘常规治疗,治疗组予常规治疗外,加用匹多莫德治疗2个月.治疗后随访观察12个月,治疗前后均监测IL-16、免疫球蛋白及淋巴细胞亚群.结果 与对照组比较,治疗组急性期病程天数、上下呼吸道感染次数、哮喘发作次数均少于对照组,差异均有统计学意义.哮喘急性发作期CD3+、CD4+、CD4+/CD8+淋巴细胞亚群较哮喘缓解期显著下降,免疫球蛋白轻度降低,IL-16较哮喘缓解期明显增高.匹多莫德治疗后3项指标均有明显改善.除IgG、IgM外,余均有统计学意义(P ＜ 0.05).结论 IL-16参与了哮喘发病的全过程,匹多莫德可下调IL-16的产生,从抗炎和提高免疫力的角度达到治疗哮喘的作用,安全有效.     

IL-12对小鼠哮喘模型Th亚群和气道炎症的影响

目的观察腹腔注射IL-12对哮喘小鼠Th亚群的调节和气道炎症的影响,并寻找更有效的干预阶段。方法将36只BALB/c小鼠分为4组,每组9只,分别为哮喘组、IL-12干预A组、IL-12干预B组及正常对照组。采用卵白蛋白(OVA)腹腔注射致敏加雾化吸入激发的方法制成哮喘模型,正常对照组小鼠同时以等量的生理盐水腹腔注射加雾化吸入。干预A组在致敏和激发阶段均给予IL-12腹腔注射进行干预,干预B组仅在激发阶段给予IL-12腹腔注射进行干预。最后1次激发结束后24h处死所有小鼠,取左肺作病理切片(HE染色),右肺提取总RNA并逆转录成cDNA后,应用半定量RT-PCR法检测肺组织内IFN-γ基因mRNA的转录表达情况,实时定量PCR法检测肺组织内IL-4基因mRNA的转录表达情况。结果与正常对照组相比,哮喘组小鼠肺组织内IFN-γmRNA表达显著减少(P<0.05),IL-4mRNA表达显著增多(P<0.05);与哮喘组相比,IL-12干预A、B组小鼠肺组织内IFN-γmRNA表达均显著增多(P均<0.05),IL-4mRNA表达均显著减少(P均<0.05)。干预A组与干预B组相比,IL-4mRNA的表达水平差异有统计学意义(P<0.05),而IFN-γmRNA表达水平差异无统计学意义(P>0.05)。结论IL-12能有效纠正哮喘小鼠失衡的Th亚群及控制气道炎症;致敏、激发阶段同时干预与仅激发阶段的干预均能有效的抑制Th2型免疫反应和气道炎症改变,前者能更有效的降低IL-4mRNA的表达水平。     

1型糖尿病患儿反复发生酮症酸中毒的原因

目的　分析 1型糖尿病患儿反复发生酮症酸中毒 (DKA)的原因。方法　回顾总结 2 0年来在我院诊治的 1型糖尿病患儿 85 0例次 ,其中因DKA住院 2 2 5例次 ,2次或 2次以上者 5 6例 ,131例次 ,将其分为前 10年和后 10年两组进行分析。结果　两组DKA患儿占总糖尿病人数比率及反复发生DKA人数相比有显著差异 ,后 10年显著少于前 10年 (P <0 .0 1)。在诱因方面感染占第 1位 ,平均 71.8% ;不控制饮食而暴饮暴食 19% ;因停用胰岛素 9.2 % ,两组相比无显著差异 (P >0 .0 5 )。结论　对糖尿病病人进行系统的管理和教育是降低DKA发生率的重要手段     

T cell subsets In peripheral blood and cerebrospinal fluid from children with aseptic meningitis

T cell subsets in peripheral blood (PB) and cerebrospinal fluid (CSF) obtained from patients with aseptic meningitis were studied using quantitative two-color fluorescence analysis with a flow cytometer. The percentage of HLA-DR⁺/CD3⁺ lymphocytes (activated T cells) in CSF was significantly increased in the recovery phase when compared to the acute phase, while no significant change in the activated T cells in PB was observed. More interestingly, CD4⁺ T lymphocytes in CSF were increased in the acute phase and subsequently decreased in the recovery phase. Instead, CD8⁺ T lymphocytes gradually accumulated into the CSF in the recovery phase, resulting in a successive decrease in the CD4/CD8 ratio. On the other hand, the CD4/CD8 ratio in PB remained normal during the course of aseptic meningitis. The present results suggest that T lymphocytes (CD4⁺ subset in the acute phase and CD8⁺ in the recovery phase) could be infiltrated and further activated at the site of inflammation, possibly in the subarachnoid space in the patients with aseptic meningitis.     

Modulation of type 1 and type 2 diabetes risk by the intestinal microbiome

The prevalence of type 1 and type 2 diabetes have both risen dramatically over the last 50 years. Recent findings point towards the gut microbiota as a potential contributor to these trends. The hundred trillion bacteria residing in the mammalian gut have established a symbiotic relation with their host and influence many aspects of host metabolism, physiology, and immunity. In this review, we examine recent data linking gut microbiome composition and function to anti‐pancreatic immunity, insulin‐resistance, and obesity. Studies in rodents and human longitudinal studies suggest that an altered gut microbiome characterized by lower diversity and resilience is associated with type 1 and type 2 diabetes. Through its metabolites and enzymatic arsenal, the microbiota shape host metabolism, energy extracted from the diet and contribute to the normal development of the immune system and to tissue inflammation. Increasing evidence underscores the importance of the maternal microbiome, the gestational environment and the conditions of newborn delivery in establishing the gut microbiota of the offspring. Perturbations of the maternal microbiome during gestation, or that of the offspring during early infant development may promote a pro‐inflammatory environment conducive to the development of autoimmunity and metabolic disturbance. Collectively the findings reviewed herein underscore the need for mechanistic investigations in rodent models and in human studies to better define the relationships between microbial and host inflammatory activity in diabetes, and to evaluate the potential of microbe‐derived therapeutics in the prevention and treatment of both forms of diabetes.     

Surface marker patterns of T cells and expression of interleukin-2 receptor in measles infection

The surface marker patterns of T cells of Ghanaian children during measles infection were studied and an attempt was made to demonstrate T cell activation and viability in vitro after activation in vivo by measles virus. The frequencies of CD4⁺ and CD8⁺ naive T cells in measles patients were high while their memory T cells were remarkably reduced with no sign of proliferation even at the acute phase of the illness. The reduction of memory T cells was prolonged during the convalescent phase (2 months after onset). The anti-CD3 monoclonal antibody-induced expression of interleukin-2 receptor α chain (IL-2R/CD25) was significantly suppressed; however, the addition of phorbol 12-myristate 13-acetate or ionomycin caused a remarkable recovery of CD25 expression. On simple culture, an appreciable proportion of T cells from measles patients died rapidly in contrast with only a few T cells from healthy controls doing so. The suppression of CD25 expression was still demonstrated during the convalescent phase of the disease. Taken together these results suggest unresponsiveness and activation-induced cell death of T cells during severe measles infection in Ghanaian children. Furthermore the prolonged abnormalities of T cells (i.e. decreased memory T cells and inhibition of CD25 expression during the convalescent phase) might be related to post-measles infection immunosuppressive status.     

Serum vitamin D levels are lower in Australian children and adolescents with type 1 diabetes than in children without diabetes

Vitamin D is synthesised in the skin through the action of UVB radiation (sunlight), and 25‐hydroxy vitamin D (25OHD) measured in serum as a marker of vitamin D status. Several studies, mostly conducted in high latitudes, have shown an association between type 1 diabetes mellitus (T1DM) and low serum 25OHD. We conducted a case–control study to determine whether, in a sub‐tropical environment with abundant sunlight (latitude 27.5°S), children with T1DM have lower serum vitamin D than children without diabetes. Fifty‐six children with T1DM (14 newly diagnosed) and 46 unrelated control children participated in the study. Serum 25OHD, 1,25‐dihydroxy vitamin D (1,25(OH)₂D) and selected biochemical indices were measured. Vitamin D receptor (VDR) polymorphisms Taq1, Fok1, and Apa1 were genotyped. Fitzpatrick skin classification, self‐reported daily hours of outdoor exposure, and mean UV index over the 35 d prior to blood collection were recorded. Serum 25OHD was lower in children with T1DM (n = 56) than in controls (n = 46) [mean (95%CI) = 78.7 (71.8–85.6) nmol/L vs. 91.4 (83.5–98.7) nmol/L, p = 0.02]. T1DM children had lower self‐reported outdoor exposure and mean UV exposure, but no significant difference in distribution of VDR polymorphisms. 25OHD remained lower in children with T1DM after covariate adjustment. Children newly diagnosed with T1DM had lower 1,25(OH)₂D [median (IQR) = 89 (68–122) pmol/L] than controls [121 (108–159) pmol/L, p = 0.03], or children with established diabetes [137 (113–153) pmol/L, p = 0.01]. Children with T1DM have lower 25OHD than controls, even in an environment of abundant sunlight. Whether low vitamin D is a risk factor or consequence of T1DM is unknown.     

Expression of T subsets and mIL-2R in peripheral blood of newborns with hypoxic ischemic encephalopathy

Background  Infantile and undifferentiated immune cells in the pathogenesis of neonates with HIE have been studied in recent years. This study was undertaken to observe the expression level of T subsets and membrane interleukin-2 receptor (mIL-2R) in the peripheral blood of newborns with hypoxic ischemic encephalopathy (HIE) and its clinical manifestations. Methods  The peripheral blood mononuclear cells (PBMCs) of newborns with HIE and normal controls were isolated by the routine Ficoll-Hypaque method, and the rates of CD₃ ⁺, CD₄ ⁺, CD₈ ⁺, CD₄ ⁺/CD₈ ⁺ and mIL-2R induced and not induced by phytohemagglutinin (PHA) were detected by biotin-streptavidin (BSA) at the first, third and seventh day after birth. Results  At the first day after birth, the positive rates of CD₃ ⁺, CD₄ ⁺, CD₈ ⁺, CD₄ ⁺/CD₈ ⁺ and mIL-2R induced and not induced by PHA were (37.4±6.7)%, (29.4±6.9)%, (16.7±3.3)%, 1.8±0.5, (3.6±1.1)% and (20.9±4.8)%, respectively. Significant differences were observed between the HIE group and the normal controls (P<0.01-P<0.05). At the third day after birth, the positive rates of CD₃ ⁺, CD₄ ⁺, CD₈ ⁺, CD₄ ⁺/CD₈ ⁺ and mIL-2R induced and not induced by PHA were (41.0±7.4)%, (35.8±6.9)%, (22.6±4.5)%, (1.7±0.5), (3.9±1.2)%, and (22.8±5.1)%, respectively. There were significant differences between the HIE group and the normal controls (P<0.05). At the seventh day after birth, the positive rates of CD₃ ⁺, CD₄ ⁺, CD₈ ⁺ were (41.8±6.1)%, (36.4±5.1)% and (25.6±4.3)%, respectively. There was significant difference between the HIE group and the normal controls (P<0.05). The ratio of CD₄ ⁺/CD₈ ⁺ and the expression level of mIL-2R induced and not induced by PHA were 1.5±0.3, (4.1±1.2)% and (23.8±5.2)%, respectively. There was no significant difference between the HIE group and the normal controls (P>0.05). Conclusions  Peripheral blood mononuclear cells of newborns are immature and undifferentiated with a very low expression level of surface markers. The changes of cell immunity involve in the pathogenesis of HIE. The disorder of cellular immune function exists in newborns with HIE. Cell immunity and immune regulative response in newborns are gradually improved or mature during the period of growing, facilitating the recovery from brain injury caused by HIE.