接种纯化人用狂犬病疫苗对妊娠期Th1/Th2类细胞因子谱的影响

目的研究人用狂犬病纯化疫苗（RV）对妊娠期Th1/Th2类细胞因子谱的影响。方法对所有可疑狂犬病毒暴露者进行RV的全程接种,在接种RV的第0、14、45天时采血并分离外周血单个核细胞与RV进行培养,采用ELISA法检测抗狂犬病病毒抗体,体外培养检测淋巴细胞增殖能力,CBA法检测细胞培养上清液中Th1类细胞因子：干扰素-γ（IFN-γ）、肿瘤坏死因子（TNF）、白细胞介素-2（IL-2）以及Th2类细胞因子：IL-4、IL-5、IL-10的水平。结果 17例暴露者于RV全程注射后17d（第45天）抗体检测阳性;RV刺激后,暴露者第45天淋巴细胞增殖能力明显高于第0天（P〈0.05）;当RV刺激后,暴露组第14天、第45天产生IL-2、IL-4、IL-5的含量显著高于未刺激组及暴露组第0天水平（P〈0.05）。结论妊娠期注射RV在刺激机体产生体液免疫的同时,可以有效地诱导Th1/Th2类细胞因子的产生。     

急性MCMV感染对小鼠脾Th1/Th2/Th17细胞亚群分化的影响

目的:在整体水平观察小鼠巨细胞病毒(MCMV)感染对小鼠脾Th1/Th2/Th17细胞亚群分化及其主要的效应性细胞因子(IFN-γ、IL-4、IL-17A)表达的影响.方法:建立MCMV感染模型,8只BALB/c小鼠分别于接种MCMV Smith株后3天和14天各处死4只;另设8只接种唾液腺匀浆的模拟感染小鼠作为对照.用空斑形成试验测定肝、脾和唾液腺组织病毒滴度;流式细胞术检测脾T淋巴细胞中Th1(CD4+ IFN-γ+)、Th2(CD4+ IL-4+)、Th17(CD4+IL-17A+)细胞比例,双抗体夹心ELISA法检测脾细胞培养上清中病毒特异性IFN-γ、IL-4、IL-17A水平.结果:MCMV感染早期肝、脾和唾液腺组织中病毒呈低水平复制,而感染后14天仅在唾液腺组织呈高水平复制;Th1细胞比例及病毒特异性IFN-γ主要在MCMV感染早期呈显著升高(P ＜0.01);Th2细胞及IL-4均无明显表达及改变;Th17细胞及病毒特异性IL-17A则主要在感染后14天升高(P＜0.05).结论:MCMV感染早期,机体通过上调Th1细胞分化比例及IFN-γ的表达发挥抗病毒效应,而MCMV诱导Th17细胞分化及IL-17A的高表达可能是MCMV感染致宿主特异性细胞免疫功能失调并逃避机体特异性细胞免疫攻击的原因之一.     

慢性乙肝患者树突状细胞对Th1/Th2分化的影响

探讨慢性乙肝患者树突状细胞(dendritic cells,DC)对CD4+Th细胞亚群分化的影响。分离慢性乙肝患者外周血单个核细胞(PBMC),以rhIL-4(50 ng/ml)、rhGM-CSF(10 ng/ml)和rhTNF-α(100 u/ml)诱导培养DC。以流式细胞仪检测DC表面CD1a、CD83、CD80、CD86、HLA-DR分子表达情况。MTT法检测DC刺激同种异体淋巴细胞增殖能力。免疫磁珠分离外周血CD4+T细胞亚群,PMA+Ionomycin刺激后胞内荧光染色,流式细胞仪检测辅助性T细胞(helper T cell,Th)内特征性细胞因子IFN-γ/IL-4以判断Th1/Th2分化。ELISA法检测DC或Th细胞培养上清中IL-6、IL-12、IFN-γ和IL-4的含量。结果:慢性乙肝患者的DC表达CD1a、CD83、CD80、CD86、HLA-DR分子水平明显低于正常人(P<0.01);培养至第7天,慢性乙肝患者DC分泌的IL-12水平低于正常人(P<0.01),而分泌的IL-6水平增高(P<0.05)。与正常人相比,慢性乙肝患者外周血中Th1细胞占CD4+T细胞的百分比较低(P<0.01),其Th细胞培养上清中IFN-γ的量也较低(P<0.01)。患者DC与同种异体的健康人Th细胞共培养,刺激Th1型细胞因子IFN-γ产生的能力低于正常人(P<0.01)。慢性乙肝患者体内DC功能的异常可能导致了外周血Th1细胞分化不足。     

结核分枝杆菌培养滤液蛋白对变应性鼻炎患者Th1和Th2失衡的影响

目的：观察结核分枝杆菌培养滤液蛋白（Mycobacterium tuberculosis culture filtrate protein，CFP）对变应性鼻炎患者Th1和Th2失衡的影响。方法：抽取30例变应性鼻炎患者外周静脉血，分离单个核细胞（PBMCs），采用MTF法测定刺激淋巴细胞增殖最佳CFP浓度，采用酶联免疫吸附试验（ELISA）检测CFP干预前后PBMCs培养上清液中的白细胞介素4（IL-4）、白细胞介素5（IL-5）和干扰素γ（IFN-γ）水平。结果：变应性鼻炎患者组PBMCs上清液中IL-4、IL-5含量较正常对照组显著增高，而IFN-γ含量显著减少。CFP干预后变应性鼻炎患者组上清液IL-4、IL-5水平明显降低，而IFN-γ含量显著升高，差异有显著性。结论：CFP能纠正变应性鼻炎患者体内Th1和Th2细胞因子的失平衡状态，为治疗变应性鼻炎提供了理论依据。     

乳杆菌对原代淋巴细胞中Th1/Th2细胞平衡的影响

目的:分析7种乳杆菌对原代淋巴细胞增殖和细胞因子(CK)分泌的作用,进而探讨其对Th1/Th2细胞平衡的影响。方法:用不同种属、不同浓度的活的/热致死的乳杆菌体外作用于小鼠脾淋巴细胞培养60 h后,采用MTT比色法检测淋巴细胞的增殖效果。用ELISA法检测Th1型细胞因子(IL-12、IFN-γ)、Th2型细胞因子(IL-4、IL-10)和调节型细胞因子(TGF-β)的分泌量。结果:活的/热致死的乳杆菌单独作用,就能促进淋巴细胞体外增殖并表现出剂量依赖关系(P<0.05)。当菌的浓度为107集落形成单位(CFU)/mL(即细菌与细胞的比例为10∶1)时,热致死的发酵乳杆菌和嗜酸乳杆菌的免疫活性近似于活菌。而且,这两株热致死菌还可适当提高淋巴细胞分泌IL-12和IFN-γ,抑制IL-4、IL-10和TGF-β的分泌,使其IFN-γ/IL-4的比值(代表Th1/Th2细胞平衡)均显著高于刀豆蛋白A(ConA)对照组(P<0.05)。结论:乳杆菌可通过提高淋巴细胞的IFN-γ/IL-4分泌率来促进Th1优势状态的Th1/Th2细胞平衡,并具有菌株特异性。     

非诺贝特通过调节Th1/Th2细胞因子的平衡改善自身免疫性心肌炎

目的探讨非诺贝特(fenofibrate)对自身免疫性心肌炎(EAM)大鼠的治疗作用。方法将提纯精制后的猪心室肌球蛋白加等体积含灭活的结核杆菌的完全弗氏免疫佐剂充分混匀后,于Lewis大鼠双后足皮下注射制作大鼠EAM模型。于第0天免疫后,非诺贝特组给予非诺贝特灌胃,EAM组给予生理盐水灌胃。免疫后的第17天,超声检测大鼠心功能,处死大鼠取心脏评估心肌炎的严重程度及心体质量比,HE染色,应用实时定量PCR检测心脏的IFN-γ,IL-2,IL-4和IL-10的mRNA表达水平,并进一步通过ELISA检测血清中IFN-γ和IL-4的表达水平。结果非诺贝特组大鼠的心功能指标与EAM组相比得到了显著改善。非诺贝特治疗组的心体质量比和心肌的炎症浸润程度也比EAM模型组有明显的降低。另外,非诺贝特治疗组降低了Th1的细胞因子(IFN-γ,IL-2)的表达并增加了Th2细胞因子(IL-4,IL-10)的表达。ELISA的结果也显示非诺贝特治疗组血清中IFN-γ的水平降低而IL-4的水平升高。结论非诺贝特治疗可能通过调节Th1/Th2细胞因子的平衡改善自身免疫性心肌炎。     

全氟化合物与儿童哮喘及Th1/Th2免疫应答平衡相关性研究

目的 采用病例对照探讨全氟化合物(PFAAS)暴露与儿童哮喘及Th1型细胞因子白细胞介素(IL)-2,干扰素(IFN)-γ和Th2型细胞因子(IL-4,IL-5)分泌水平的关系.方法 选择231名台北医院就诊的哮喘儿童作为病例组,来自社区的225名自然儿童作为对照组.采用双抗体酶联免疫吸附实验(ELISA)试剂盒检测儿童血清中细胞因子IL-2、IFN-γ、IL-4和IL-10的分泌水平;高效液相色谱仪分析血清中全氟辛烷磺酸(PFOS)和全氟辛酸(PFOA)水平.结果 哮喘儿童机体PFOS(33.9μg/L比28.9 μg/L)和PFOA(1.2μg/L比0.5 μg/L)暴露负荷显著的高于对照组儿童,且随着机体PFAAs的增高,儿童患有哮喘的风险呈增高趋势.对哮喘儿童而言,血清PFAAs水平与Th1型细胞因子(IL-2,IFN-γ)存在显著的负相关,而与Th2型细胞因子(IL-4,IL-5)呈正相关关系.结论 PFOS暴露可诱导机体免疫应答平衡紊乱,并向Th2型免疫应答极化.     

CD86协同刺激信号在孕早期母—胎界面Th1／Th2型细胞因子表达调控中的作用

目的探讨CD86协同刺激信号在孕早期母-胎界面Th1/Th2型细胞因子表达调控中的作用。方法建立正常妊 娠模型CBA×Balb/c和自然流产模型CBA× DBA/2。于孕第4、6、8、10天给CBA孕鼠腹腔注射大鼠IgG作为对照组;仅于孕第4 天或于孕第4、6、8、10天给CBA孕鼠腹腔注射大鼠抗小鼠CD86 mAb。孕第14天计算两种模型各实验组胚胎吸收率R。ELISA 法测定孕第9和第14天各实验组母-胎界面组织体外培养上清中Th1/Th2型及相关细胞因子(IL-2、IFN-γ、TNF-α、IL-4、IL-10、 TGF-β2)表达水平。结果孕早期干预CD86协同刺激信号,对正常妊娠模型母-胎界面孕第9和第14天IL-4、IL-10、TGF-β2以及 IFN-γ、TNF-α表达均无显著影响,其胚胎吸收率亦无显著变化。自然流产模型中,孕早期干预CD86协同刺激信号后,孕第9、 第14天母-胎界面IL-4、IL-10、TGF-β2表达均显著增加(P＜0.05);而IFN-γ、TNF-α表达显著下降(P＜0.05)。胚胎吸收率亦 显著下降(P＜0.05)。结论孕早期母-胎界面CD86协同刺激信号的调节紊乱可能是触发母体对胚胎产生免疫排斥的重要病 理因素,于孕早期干预CD86协同刺激信号能够恢复母-胎界面Th1型/Th2型免疫调节的生理平衡,从而诱导母-胎免疫耐受。     

不同级别胶质瘤患者术前外周血Th1/Th2细胞因子的表达

目的:分析不同级别脑胶质瘤患者手术前外周血Th1/Th2细胞因子表达变化。方法:选择近期住院的脑胶质瘤患者63例,在治疗前采用ELISA方法进行外周血IFN-γ、IL-2、IL-4和IL-10浓度检测。结果:胶质瘤组外周血IL-4和IL-10浓度均明显高于对照组,而前者外周血IFN-γ、IL-2浓度及IFN-γ/IL-4比值则显著低于后者(P<0.05或P<0.01)。高级别组(Ⅲ~Ⅳ级)外周血IL-4和IL-10浓度均明显高于低级别组(Ⅰ~Ⅱ级),而前者外周血IFN-γ、IL-2浓度及IFN-γ/IL-4比值则显著低于后者(P<0.05或P<0.01)。结论:脑胶质瘤患者可能有Th2优势表达,与恶性程度有一定关系。     

腹泻型肠易激综合征患者外周血Th1/Th2细胞因子失衡表达的分析

目的:分析腹泻型肠易激综合征(IBS)患者外周血Th1/Th2细胞因子失衡表达。方法:连续选择近期就诊的腹泻型IBS患者27例,对照组为31例同龄、同性别的同期健康体检者。两组对象接受了外周血Th相关细胞因子γ-干扰素(IFN-γ)、白细胞介素-4(IL-4)检测,并计算IFN-γ/IL-4比值。结果:腹泻型IBS组外周血IFN-γ浓度及IFN-γ/IL-4比值均明显高于对照组,而血清IL-4浓度则显著低于后者(P均<0.05～0.01)。结论:腹泻型IBS患者存在明确Th1优势失衡表达。     

CCK-8对KLH免疫小鼠脾细胞Th1/Th2平衡的影响

目的： 探讨八肽胆囊收缩素（CCK-8）对Th1/Th2平衡的调节作用。方法: 给予BALB/c小鼠钥孔戚血蓝蛋白（KLH）免疫同时体内给予不同剂量的CCK-8,酶联免疫吸附试验(ELISA)检测其脾细胞培养上清中Th1型细胞因子γ-干扰素(IFN-γ)、白细胞介素-2（IL-2）和Th2型细胞因子白细胞介素-4（IL-4）、白细胞介素-5（IL-5）水平,逆转录聚合酶链式反应(RT-PCR)法检测脾细胞中IFN-γ、IL-2、IL-4、IL-5 mRNA表达;ELISA法检测血清中Th1型抗KLH抗体IgG2a和Th2型抗KLH抗体IgG1水平。结果: ①KLH免疫使小鼠脾细胞分泌Th1/Th2型细胞因子水平明显增高,mRNA表达增高,KLH免疫同时给予CCK-8可使脾细胞培养上清中IFN-γ、IL-2含量进一步增加和IFN-γ、IL-2mRNA表达增高,而使IL-4、IL-5含量降低,IL-4、IL-5 mRNA表达减低和降低IL-4/IFN-γ比值。②KLH免疫小鼠血清中IgG2a、IgG1发生不同程度增高,CCK-8可使其血清中IgG1水平减低而使IgG2a水平增高。结论: CCK-8可促进KLH免疫小鼠体内Th1反应,使Th2优势反应向Th1方向转变。     

Th1/Th2 cytokine responses following HIV-1 immunization in seronegative volunteers

The Th1/Th2 profile that follows human vaccination may profoundly influence the subsequent course of disease after infection. However, the ability to detect IL-4 has been limited outside trials of live vaccination. By using methods in which memory effector cells are allowed to antigenically expand by short term culture, followed by low-dose mitogenic stimulation, we have been able to follow the Th1/Th2 profile in HIV-1^?volunteers enrolled in two phase I studies of HIV immunogens (a recombinant gp120 and a multivalent, octomeric V3 loop peptide). Antigen-specific interferon-gamma (IFN-γ) could be detected in primary stimulation, but IL-4 was observed only after antigenic expansion and restimulation. In both of these studies the responses after initial immunizations were dominated by IFN-γ, with IL-4 appearing only after multiple rounds of immunization, and IL-4 was temporally related to antibody production. Concomitant with the IL-4 production, the amount of supernatant IFN-γ declined. Antigen-specific IL-10 was not detected in either study. Such techniques, which have been shown to correlate with outcomes in immunotherapy, may prove useful as future surrogates of human vaccine response.     

Conversion in vivo from an early dominant Th0/Th1 response to a Th2 phenotype during the development of collagen-induced arthritis

Over the past decade, the central role of T cells in the process of collagen-induced arthritis (CIA) has been extensively documented. The inflammatory features of CIA and its successful modulation after treatment in vivo with Th2 lymphokines, known to down-regulate proinflammatory cytokines, classify CIA as a Th1-mediated disease. However, no direct evidence for the presence of the different T helper subsets has been obtained. To identify the collagen-specific CD4⁺ T cell subset(s) developing during the course of CIA, lymph nodes from susceptible DBA/1 mice (H-2q) were harvested at different times after injection of bovine type II collagen in Freund's complete adjuvant and checked by enzyme-linked immunospot assay for the production of interferon (IFN)-γ and interleukin (IL)-4. The results clearly showed that type II collagen-specific T cells secreting either IFN-γ, IL-4, or both, develop early in vivo, before the onset of arthritis: the number of IFN-γ-secreting cells was already maximal 15 days after immunization, whereas more IL-4-secreting cells were found at day 30, just before the onset of clinical arthritis. Another strategy was to establish collagen-specific CD4⁺ T cell lines and sublines in vitro and to analyze their lymphokine secretion pattern. Lines generated 8 days after immunization displayed a mixed lymphokine secretion pattern characteristic of Th0 cells or of a mixture of Th1 and Th2 cells. After limiting dilution of a day 8 line, 60% of the growing sublines were Th0-like (secreting IFN-γ, IL-4, and IL-5), and 25% were Th1 (secreting IFN-γ). By day 25 post-immunization, 33% of the generated sublines were Th0-like, 11% Th1, and 56% Th2 (secreting IL-4 and IL-5). Moreover, all the sublines raised from the lymph nodes of arthritic mice harvested at day 55 secreted high amounts of Th2 lymphokines, and only 3 out of 14 also produced some IFN-γ. This study demonstrates that during the course of CIA the collagen-specific CD4⁺ T cell response shifts in vivo from a dominant Th0/Th1 response to a clear Th2 phenotype. These results contribute to our understanding of the collagen-specific CD4⁺ T helper subsets which develop during the induction and clinical phases of CIA.     

Development in vitro of human CD4+ thymocytes into functionally mature Th2 cells. Exogenous interleukin-12 is required for priming thymocytes to produce both Th1 cytokines and interleukin-10

Fresh postnatal thymocyte cell suspensions were directly cloned under limiting dilution conditions with either phytohemagglutinin or toxic shock syndrome toxin-1 (TSST-1), a bacterial superantigen. Cultures contained allogenic irradiated feeder cells and interleukin (IL)-2, in the absence or presence of exogenous IL-4, interferon (IFN)-γ or IL-12. The resulting CD4⁺ T cell clones generated under these different experimental conditions were then analyzed for their ability to produce IL-2, IL-4, IL-5, IL-10, IFN-γ and tumor necrosis factor (TNF)-β in response to stimulation with phorbol 12-myristate 13-acetate (PMA)+anti-CD3 monoclonal antibody or PMA + ionomycin. Different from T cell clones generated from peripheral blood, virtually all CD4⁺ T cell clones generated from human thymocytes produced high concentrations of IL-2, IL-4 and IL-5, but no IFN-γ, TNF-β or IL-10. Moreover, after activation, these clones expressed on their surface membrane both CD30 and CD40 ligand, but not the product of lymphocyte activation gene (LAG)-3, and provided strong helper activity for IgE synthesis by allogeneic B cells. The Th2 cytokine pattern could not be modified by the addition of IFN-γ. However, upon addition of exogenous IL-12, the resulting CD4⁺ thymocyte clones produced TNF-β, IFN-γ, and IL-10 in addition to IL-4 and IL-5. These results suggest that CD4⁺ human thymocytes have the potential to develop into cells producing the Th2 cytokines IL-4 and IL-5, whereas the ability to produce both Th1 cytokines and IL-10 is acquired only after priming with IL-12.     

IFN-γ上调Th17/IL-17应答介导衣原体呼吸道感染免疫保护

目的 探讨IFN-γ在小鼠沙眼衣原体感染中对Th17/IL-17应答的调节作用.方法 利用沙眼衣原体鼠肺炎株小鼠呼吸道感染模型,用抗鼠IFN-γ单克隆抗体吸入中和肺组织IFN-γ,对照组给予同等剂量的独特型抗体IgG2a,于感染后7 d处死小鼠.免疫酶法检测小鼠肺组织衣原体生长;利用RT-PCR技术检测衣原体感染小鼠肺组织中Th17相关因子IL-17及其上游因子IL-23 mRNA的表达;细胞内细胞因子染色检测衣原体感染小鼠脾脏IL-17-CD4+T细胞的扩增.结果 与对照组相比,IFN-γ抗体中和小鼠有严重的疾病状态,包括明显的体重下降、肺组织更高的衣原体负荷和肺组织更严重的病理损伤;肺组织IL-17和IL-23 mRNA的表达水平显著降低;脾脏IL-17-CD4+T细胞百分率也显著降低.结论 小鼠衣原体感染中,IFN-γ通过上调Th17/IL-17应答起保护作用.

Abstract：

Objective To investigate the regulation of IFN-γ to Th17 response in Chlamydia muridarum (Cm) lung infection in mice. Methods A murine model of pneumonia induced by intranasal inoculation of Cm was used for this study. Anti-mouse IFN-γ McAbs were used to neutralize endogenous IFN-γfollowing Cm lung infection. Control group received the same dose of isotype antibody (IgG2a). Mice were sacrificed at day 7 postinfection. Chlamydial growth in the lung was assessed by immunoenzyme technique.IL-17 and IL-23 mRNA expression in the lung was assayed by RT-PCR and the proliferation of IL-17 + CD4 +T cells in the spleen was assayed by intracellular cytokine staining. Results IFN-γ-neutralized mice exhibited serious disease course, include greater body weight loss, higher organism growth and much more severe pathological changes in the lung compared with control mice. The mRNA expression of IL-17 and IL-23 in the lung and the proliferation of IL-17 + CD4 + T cells in the spleen significantly decreased in the IL-17- neutralized mice. Conclusion IFN-γ was protective in Cm lung infection through up-regulating the antigen specific Th17 responses.     

不明原因习惯性流产患者主动免疫治疗前后Th1/Th2型细胞因子水平的变化

为探讨主动免疫治疗对不明原因习惯性流产 (UHA )患者Th1/Th2型细胞因子水平的影响。采用酶联免疫吸附法检测15例正常非妊娠妇女、 35例UHA患者淋巴细胞主动免疫治疗前后经滋养细胞抗原刺激的外周血单个核细胞 (PBMC )培养上清液中IL 2、IFN γ、IL 4、IL 10的水平。结果发现 :(1)在最佳诱导时间下 ,UHA组治疗前PBMC产生IL 2、IFN γ的水平明显高于正常对照组 (P <0 0 5 ) ,IL 4、IL 10水平明显低于正常对照组 (P <0 0 5 )。UHA组治疗后PBMC产生IL 2、IFN γ的水平较治疗前明显降低 (P <0 0 5 ) ,IL 4、IL 10水平较治疗前明显升高 (P <0 0 5 )。UHA组治疗后PBMC产生各细胞因子的水平与正常对照组比较 ,差异均无显著性 (P >0 0 5 ) ;(2 )UHA组 35例患者主动免疫治疗后半年内 2 8例妊娠 ,其中 9例又出现自然流产。 9例自然流产者治疗后IL 2、IFN γ水平未明显下降 ,IL 10水平未明显上升。 19例妊娠成功者治疗后IL 2、IFN γ水平较治疗前明显下降 (P <0 0 5 ) ,IL 4、IL 10水平明显上升 (P <0 0 5 )。以上结果表明UHA患者对滋养细胞抗原产生以Th1型反应为主的免疫应答 ,产生大量Th1型细胞因子 ,主动免疫治疗有助于上调Th2型细胞因子及下调Th1型细胞因子 ,利于UHA患者妊娠成功。     

纠正Th1/Th2迁移在小儿过敏性紫癜早期肾损伤急救中的临床意义

目的研究并探讨纠正Th1/Th2迁移在小儿过敏性紫癜早期肾损伤急救中的临床意义。 方法选取2012年1月至2015年1月于商丘市第一人民医院被确诊为小儿过敏性紫癜且发生早期肾损伤的50例患儿作为研究对象,命名为紫癜性肾炎组,另选取同期就诊的50例未发生肾损伤的小儿过敏性紫癜患儿和同期进行体检的50例健康体检儿,分别命名为单纯紫癜组、对照组,仅紫癜性肾炎组患儿给予纠正Th1/Th2迁移治疗。各组治疗前后采用流式细胞仪检测Th1、Th2细胞的比例、ELISA法测定白细胞介素-4(IL-4)、γ-干扰素(IFN-γ)含量、免疫比浊法检测尿微量蛋白含量。 结果治疗前,紫癜性肾炎组与单纯紫癜组IL-4、IFN-γ、Th1、Th2差异均无统计学意义(P>0.05),但两组的IFN-γ、Th1、Th1/Th2均较对照组明显更低,IL-4、Th2均较对照组明显更高,差异均有统计学意义(P<0.05)。与治疗前相比,紫癜性肾炎组患儿治疗后的IFN-γ、Th1、Th1/Th2均明显提升高,IL-4、Th2均明显降低,差异均有统计学意义(P<0.05),且与对照组比较差异均无统计学意义(P>0.05),紫癜性肾炎组尿微量蛋白含量得到显著改善(P<0.05)。 结论给予小儿过敏性紫癜早期肾损伤患儿纠正Th1、Th2迁移治疗,可有效纠正Th1/Th2失衡,Th1/Th2可作为判断小儿过敏性紫癜病情进展及其早期肾损伤预后的重要指标。