一种根瘤菌胞外多糖对小鼠免疫功能的影响

目的研究一种根瘤菌胞外多糖(REPS)对正常小鼠免疫功能的影响。方法将该多糖以大、中、小3个剂量[(40、20、10 mg/(Kg.d)]给小鼠连续腹腔注射(ip)10 d,测定胸腺质量、脾脏质量、碳粒廓清指数、血清抗绵羊红细胞(SRBC)抗体凝集效价和淋巴细胞转化值。结果与对照组比较,该多糖使小鼠脾脏质量明显增加,单核吞噬细胞的吞噬能力显著增强,提高了血清抗SRBC抗体凝集效价,增强了小鼠脾淋巴细胞转化功能。结论此根瘤菌胞外多糖对小鼠的非特异性和特异性免疫功能均有明显的增强作用。     

小儿慢性乙型肝炎外周血T细胞亚群和临床病理关系的研究

目的　探讨小儿慢性乙型肝炎细胞免疫功能与临床、病理的关系 ,了解其间的相关性。方法　研究对象为确诊的 94例 12岁以内慢性乙型肝炎住院患儿。常规检测血T细胞亚群等、血丙氨酸转氨酶 (ALT)水平、病毒学指标 ,并进行腹部B超、肝脏病理学检查。结果　有活动性肝脏病理炎症者CD4 CD8 升高 (P <0 0 5 ) ;女性比男性CD4 降低差异有非常显著意义 (P <0 0 1)、CD8 升高差异有显著意义 (P <0 0 5 )、CD4 CD8 降低差异有非常显著意义 (P <0 0 1) ;T淋巴细胞的异常改变与HBVDNA、PTA以及脾脏大小关系不明显。而各项观察的临床、病理指标与CD3 T淋巴细胞、B淋巴细胞均无明显相关性。结论　小儿慢性乙型肝炎患者机体存在细胞免疫功能失衡 ,其相关性表现在肝脏炎症损伤严重程度与T淋巴细胞功能的损伤有明显的相关性 ,女性对HBV的T淋巴细胞反应比男性更有利于清除HBV ,其预后及对抗病毒和免疫调节治疗反应较好。     

ELISPOT,MHC肽五聚体和ICCD三种检测特异性细胞免疫应答方法的比较研究

目的 比较三种特异性细胞免疫应答的检测方法，寻求一种简便、重复性好、易于质控的评价疫苗细胞免疫的检测方法。方法采用HIV DNA疫苗肌内注射BALB／c小鼠，第6周用艾滋病重组MVA痘苗病毒腹腔注射加强免疫，于第10天制备脾脏细胞悬液，并用酶联免疫斑点法（Enzymeunked Immune Spot，EusPOT）、MHC肽五聚体法和胞内细胞因子染色分析法（Intra—cellular cytokinede tection，ICCD）分别检测细胞免疫应答。结果 ELISPOT、MHC肽五聚体染色以及胞内细胞因子染色分析法检测疫苗组细胞免疫应答的阳性率分别为5／5、4／5和3／5；而且ELISPOT和MHC肽五聚体染色法之间有一定相关性（r=0、647），而ELISPOT和胞内因子染色法之间以及MHC肽五聚体染色和胞内因子染色之间无相关性。结论ELISPOT试验操作相对简单，灵敏度高、重复性好，是评价疫苗细胞免疫的有效方法。     

β-casomorphin-7对小鼠的免疫调节作用

目的：通过体外和体内方法研究β-casomorphin-7对小鼠脾脏淋巴细胞和腹腔巨噬细胞的作用.方法：利用脾细胞增殖试验和腹腔巨噬细胞中NO浓度的变化来研究体外不同的β-casomorphin-7浓度对脾脏淋巴细胞的增殖和腹腔巨噬细胞中NO浓度变化的影响,以及腹腔注射β-casomorphin-7和饮用β-casomorphin-7溶液对上述两个指标的影响.结果：体外试验表明,β-casomorphin-7在不同浓度对脾脏淋巴细胞的增殖显示了刺激和抑制的双向作用,而对NO的产生显示了明显的抑制作用（P＜0.01）.体内试验表明,β-casomorphin-7通过腹腔注射和饮用两种给药方式对脾淋巴细胞和腹腔巨噬细胞的作用是一致的.β-casomorphin-7显著地增强了脾淋巴细胞的增殖反应（P＜0.01）,且抑制了腹腔巨噬细胞NO的产生.结论：当前的试验表明,β-casomorphin-7具有免疫调节作用,且小鼠在2～3周龄时,可吸收入血发挥免疫调节作用.     

Regulatory effects of osteoprotegerin on cellular and humoral immune responses

The interaction between receptor activator of nuclear factor-kappaB ligand (RANKL) and RANK has been reported to regulate immunity in addition to bone metabolism. The aim of this study was to determine if osteoprotegerin (OPG), an inhibitor of the RANKL-RANK interaction and possibly a new drug against osteoporosis, would adversely affect immunity. OPG was used to treat mice developing different models of cellular and humoral immune responses and also in vitro in T and B cell assays. In mice, OPG does not affect cell-mediated reactions such as contact hypersensitivity to the hapten oxazolone and liver damage, granuloma formation, and infectious load induced by mycobacterial infection. However, OPG increases humoral reactions such as the production of IgM, IgG, and IgE against the T cell dependent antigen keyhole limpet hemocyanin and the production of IgM against the T cell independent antigen Pneumovax. In vitro, OPG modestly co-stimulates T cells but does not affect the proliferation of B cells. OPG has modest immunoregulatory effects that seem to be confined to the humoral response to specific antigens.     

Extensive immune-mediated hippocampal damage in mice surviving infection with neuroadapted Sindbis virus

Viral infections of the central nervous system and immune responses to these infections cause a variety of neurological diseases. Infection of weanling mice with Sindbis virus causes acute nonfatal encephalomyelitis followed by clearance of infectious virus, but persistence of viral RNA. Infection with a neuroadapted strain of Sindbis virus (NSV) causes fatal encephalomyelitis, but passive transfer of immune serum after infection protects from fatal disease and infectious virus is cleared. To determine whether persistent NSV RNA is associated with neurological damage, we examined the brains of recovered mice and found progressive loss of the hippocampal gyrus, adjacent white matter, and deep cerebral cortex associated with mononuclear cell infiltration. Mice deficient in CD4(+) T cells showed less tissue loss, while mice lacking CD8(+) T cells showed lesions comparable to those in immunocompetent mice. Mice deficient in both CD4(+) and CD8(+) T cells developed severe tissue loss similar to immunocompetent mice and this was associated with extensive infiltration of macrophages. The number of CD4(+) cells and macrophage/microglial cells, but not CD8(+) cells, infiltrating the hippocampal gyrus was correlated with the number of terminal deoxynucleotidyltransferase-mediated dUTP nick end-labeling positive pyramidal neurons. These results suggest that CD4(+) T cells can promote progressive neuronal death and tissue injury, despite clearance of infectious virus.     

Antigenic sites of coxsackie A9 virus inducing neutralizing monoclonal antibodies protective in mice

A panel of murine IgG monoclonal antibodies (MAbs) was produced against coxsackievirus A9 (CAV9). Fifty-nine MAbs reactive in ELISA with purified CAV9 were identified. Eighteen of them could efficiently inhibit infection by CAV9 but not coxsackieviruses B. Neutralization-resistant CAV9 variants to four different MAbs were isolated and tested for resistance to neutralization by other MAbs of the panel. Three groups of reactivity including 10, 7, and 1 MAbs were thus identified. Sequencing of neutralization-escape virus mutants showed that neutralization by one MAb group was affected by change of VP3 amino acids 62 or 69. For the second group of reactivity, mutations included amino acids 154 or 165 of VP2. The only MAb of the third group selected for a change at residue 70 of VP2. Protection studies in a newborn mouse model of myositis suggested that either epitopes in VP2 or in VP3 mediate protection from CAV9 infection in vivo.     

EBV感染患儿临床特征及血清免疫因子水平

目的分析124例巴尔病毒(EBV)感染患儿的临床特征和血清免疫因子水平。方法选择2016年12月-2019年12月于海南医学院第一附属医院确诊的124例EBV感染患儿为研究组,根据临床表现分为传染性单核细胞增多症(IM)组43例和单纯性EBV组81例,选择同期健康体检儿童62名为对照组。记录所有患儿入组时的年龄、性别、临床症状;荧光定量PCR反应检测外周血淋巴细胞中EBV DNA载量;检测血清白细胞介素-6(IL-6)、IL-2和肿瘤坏死因子-α(TNF-α)水平,流式细胞仪分析外周血T淋巴细胞水平;Pearson相关性分析外周血T淋巴细胞亚群与EBV DNA载量之间的相关性。结果 IM组患儿的年龄为(5.13±1.56)岁,大于单纯性EBV组(P<0.05),出现发热、咽峡炎、淋巴结肿大、脾肿大、肝肿大、眼睑水肿、鼻塞、打鼾的比例为88.37%、93.02%、93.02%、48.84%、60.47%、32.56%、55.81%和46.51%,高于单纯性EBV组(P<0.05);IM组患儿的血CD3+T、CD8+T细胞、IL-6、TNF-α为分别为(73.25±7.16)%、(40.19±4.21)%、(33.68±5.71)ng/L、(72.52±11.26)ng/L高于对照组,而CD4+T、CD4+/CD8+T细胞、IL-2分别为(34.86±3.75)%、(0.89±0.15)、(10.43±3.38)ng/L则均低于对照组(P<0.05);外周血CD3+T和CD8+T细胞水平均与病毒载量呈正相关(r=0.314,0.447,P<0.05),CD4+T和CD4+/CD8+T细胞水平与病毒载量呈负相关(r=-0.425,-0.376,P<0.05)。结论 EBV感染患儿的临床症状和细胞免疫功能与病毒载量有关,有望应用于临床评估EBV感染的病情发展。     

Scientific connotation of “treating different diseases with the same method” from the perspective of metabolic–immune dysregulation in inflammation-mediated carcinogenesis of digestive organs

Inflammation-mediated carcinogenesis develops in the context of chronic inflammation and is a significant cause of cancer within the digestive system. In the chronic inflammation microenvironment, the metabolic activity of tissue cells undergoes extensive changes, which interfere with the normal function of immune cells. Dysregulation of cell metabolism and immune function has been identified as a key factor contributing to inflammation-mediated carcinogenesis within the major digestive organs, such as the stomach, liver, and colorectum. This metabolic–immune imbalance also corresponds to traditional Chinese medicine (TCM) theories of “yin-yang disharmony” and “disharmony between Ying-nutrients and Wei-defense.” The metabolic–immune imbalance has also been regarded as the key factor supporting “treatment of different diseases with the same method,” in which the same approach is adopted in the treatment of different conditions. In the TCM treatment process, it is necessary to first identify TCM patterns and then apply the corresponding TCM to correct the dysregulated metabolic and immune function, thereby blocking the progression from inflammation to malignancy. Our study findings deepen the TCM understanding of metabolic–immune dysregulation and the relationship between metabolic–immune dysregulation, pattern identification, and treatment method. They also provide new insights for the treatment of inflammation-mediated carcinogenesis in major digestive organs and help us further explore the scientific connotation of the TCM strategy of “treating different diseases with the same method.