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目的探讨骨关节炎严重程度与血清白介素4（IL-4）和人可溶性IL-4受体（s IL-4R）的相关性。方法选择2011年5月-2013年5月收治的50例骨关节炎患者（观察组）,另选择同期50例健康体检者（对照组）,采用ELISA法检测两组血清IL-4和s IL-4R水平并进行组间比较。采用K＆L评级法和WOMAC骨关节炎指数评价观察组患者骨关节炎严重程度,并分析其与血清IL-4和s IL-4R水平的关系。结果观察组血清s IL-4R水平（82.12±11.24ng/ml）显著高于对照组（30.67±5.23ng/ml）,差异有统计学意义（P〈0.05）,但两组血清IL-4水平（分别为14.39±7.14、15.23±6.28ng/L）比较差异无统计学意义（P〉0.05）。观察组患者血清s IL-4R水平与WOMAC指数呈正相关（r=0.313,P〈0.05）;随K＆L分级增加,血清s IL-4R水平逐渐递增,各分级比较差异有统计学意义（P〈0.05）。结论血清s IL-4R水平与骨关节炎严重程度相关,临床可以将其作为评估骨关节炎严重程度的指标。

目的从单个T细胞水平探讨多发性硬化患者病程不同阶段外周血细胞因子分泌变化,以为鉴别诊断和判断病情提供线索。方法采用酶联免疫斑点试验（ELISPOT）检测外周血单个核细胞在自分泌状态下和经外源性抗原（刀豆蛋白A、髓鞘碱性蛋白、乙酰胆碱受体）刺激后,外周血白细胞介素（IL）-4、10和干扰素-γ（IFN-γ）分泌变化。结果与正常对照组和其他非免疫性神经疾病组相比,多发性硬化组患者经髓鞘碱性蛋白刺激后外周血IL-4、IL-10和IFN-γ分泌水平升高（均P=0.000）,其中髓鞘碱性蛋白特异性IFN-γ分泌水平在急性发作期或加重期高于稳定期（P=0.002）,而IL-4和IL-10则无明显改变。结论在外源性抗原髓鞘碱性蛋白刺激下,采用ELISPOT法检测多发性硬化患者血清IL-4、IL-10和IFN-γ特异性分泌水平,具有鉴别诊断和判断疾病进展阶段的作用。

目的探讨原发性。肾病综合征患儿治疗前外周血白细胞介素-4（IL-4）、γ-干扰素（IFN-γ）与激素治疗效应的关系。方法31例原发性肾病综合征患儿于治疗前抽取静脉血分离单个核细胞，加入植物血凝素刺激其生长，取其上清液，用酶联免疫吸附双抗夹心法检测IL-4、IFN-γ，激素治疗8周后根据治疗反应分为激素敏感组（17例）及激素耐药组（14例）。20例健康儿童作为对照组。结果原发性。肾病综合征中激素敏感组治疗前外周血IL-4水平明显高于激素耐药组（P〈0．01）；IFN-γ水平在激素敏感组及激素耐药组之间差异无统计学意义（P〉0．05）。结论测定。肾病综合征患儿治疗前外周血中的IL-4可以作为预测激素疗效的一项指标。

R581.4

近年来肺癌的发病率和死亡率呈明显上升趋势，严重威胁着人民的健康。在肺癌的综合治疗中，化疗起着不可替代的作用，然而，肺癌细胞多药耐药性(MDR)的产生，严重制约了肺癌化疗的效果，是引起肺癌化疗失败的关键因素。肺癌细胞多药耐药性是目前临床难以克服的课题之一，研究其产生机制并进一步寻求逆转方法，从而选择有针对性的化疗药物是临床迫切需要的。近年研究表明，rhIL-4能诱导癌细胞分化，增加某些肿瘤细胞对化疗药物的敏感性，从而降低MDR。

Our previous salivary study had demonstrated an apparent T helper 2 （Th2）-predominance in saliva of oral lichen planus （OLP） patients and suggested a potential of salivary interleukin-4 （IL-4） as a biomarker for monitoring disease severity. To further determine the consistency of Th1/Th2 bias of OLP, this study investigated the expression profile of interferon-γ （IFN-γ） and IL-4 in serum and the relationship of the serum levels of these cytokines with their saliva partners. Sixty ethnic Chinese patients with OLP （40 of the erythematous/ulcerative form and 20 of the reticular form） were recruited for this study, with 40 age-sex-matched healthy volunteers as control group. IFN-γ and IL-4 levels in serum and paired saliva samples were screened by enzyme-linked immunosorbent assay. OLP patient showed a low-level IFN-γ but high-level IL-4 expression profile in both serum and saliva, with a lower IFN-γ/IL-4 ratio. Serum IL-4 level in the erythematous/ulcerative group was significantly higher than that in the reticular group. Serum levels of IFN-γ and IL-4 were significantly and positively correlated with their saliva partners. These results provided more evidence for Th2 cytokine- predominant immune imbalance in OLP, as well as the potential of IL-4 as the biomarker for monitoring severity of OLP.

High salt is positively associated with the risk of many diseases. However, little is known about the mechanisms. Here we showed that high salt increased proinflammatory molecules, while decreased anti-inflammatory and pro- endocytic molecules in both human and mouse macrophages. High salt also potentiated lipopolysaccharide-induced macrophage activation and suppressed interleukin 4-induced macrophage activation. High salt induced the proinflammatory aspects by activating p38/cFos and/or Erkl/2/cFos pathways, while inhibited the anti-inflammatory and proendocytic aspects by Erkl/2/signal transducer and activator of transcription 6 pathway. Consistent with the in vitro results, high-salt diet increased proinflammatory gene expression of mouse alveolar macrophages. In mouse models of acute lung injury, high-salt diet aggravated lipopolysaccharide-induced pulmonary macrophage activation and inflammation in lungs. These results identify a novel macrophage activation state, M（Na）, and high salt as a potential environmental risk factor for lung inflammation through the induction of M（Na）.

Interleukin 4 （IL-4） has a variety of immune functions, including helper T-cell （Th-cell） differentiation and innate immune-response processes. However, the impact of IL-4 on gamma delta （γδ） T cells remains unclear. In this study, we investigate the effects of IL-4 on the activation and proliferation of γδ T cells and the balance between variable delta 1 （Vδ1） and Vδ2 T cells in humans. The results show that I L-4 inhibits the activation of y8 T cells in the presence of γδ T-cell receptor （TCR） stimulation in a STAT6-dependent manner. IL-4 promoted the growth of activated γδ T cells and increased the levels of Vδ1 T cells, which in turn inhibited V82 T-cell growth via significant IL-10 secretion. VδI T cells secreted significantly less interferon gamma （IFNy） and more IL-10 relative to Vδ2. Furthermore, Vδ1 T cells showed relatively low levels of Natural Killer Group 2D （NKG2D） expression in the presence of IL-4, suggesting that Vδ1 T cells weaken the γδ T cell-mediated anti-tumor immune response. For the first time, our findings demonstrate a negative regulatory role of IL-4 in γδ T cell-mediated anti-tumor immunity.

Parkinson＇s disease （PD） has been described as one of the most common neurodegenerative diseases affecting up to 2% of the worldwide population over 60 years of age. The hallmarks of PD are progressive loss of midbrain dopaminergic （mDA） neurons and a decrease in striatal dopamine levels, which result in typ- ical clinical motor symptoms such as akinesia, resting tremor, rigidity, and gait impairments. Although the causes for PD are only partially understood and seem to be very heterogeneous, one of the common phenomenons observed in toxin-based an- imal models of PD as well as PD patients is a microglia-driven neuroinflammatory response,

This study assessed and compared the immunogenicity of various immunization strategies in mice using combinations of re- combinant DNA （pCCMp24） and recombinant attenuated vaccinia virus Tian Tan （rddVTT_ccMpe4）. Intramuscular immuniza- tion was performed on days 0 （prime） and 21 （boost）. The immunogenicity of the vaccine schedules was determined by meas- uring human immunodeficiency virus （HIV）-specific binding antibody levels and cytokine （interleukin-2 and interleukin-4） concentrations in peripheral blood, analyzing lymphocyte proliferation capacity against HIV epitopes and CD4~/CD8＋cell ratio, and monitoring interferon-gamma levels at different times post-immunization. The results showed that pCCMp24, rddVTT.ccMp24 and their prime-boost immunization induced humoral and cellular immune responses. The pCCMp24/ rddVTT.ccMp24 immunization strategy increased CD8＋ T cells and induced more IFN-7-secreting cells compared with sin- gle-shot rDNA. The prime-boost immunization strategy also induced the generation of cellular immunological memory to HIV epitope peptides. These results demonstrated that prime-boost immunization with rDNA and rddVTT_ccMp24 had a tendency to induce greater cellular immune response than single-shot vaccinations, especially IFN-7 response, providing a basis for further studies.