国产利福平对小鼠细胞免疫反应的抑制作用

利福平在体外高度地抑制由有丝分裂原和特异性抗原诱导的致敏和非致敏小鼠脾淋巴细胞转化,其抑制作用与利福平的浓度相关,也与其加入至培养物的时间相关.利福平对小鼠腹腔巨噬细胞产生白细胞介素1的能力和小鼠胸腺细胞对白细胞介素1的反应也有抑制作用,其抑制作用也与利福平的浓度成良好的量效关系.     

COMBINED IL-2/IL-3 GENE THERAPY FOR G422 MOUSE GLIOBLASTOMA BY INTRATUMORAL INJECTION OF RECOMBINANT ADENOVIRUSES

ＣＯＭＢＩＮＥＤＩＬ２／ＩＬ３ＧＥＮＥＴＨＥＲＡＰＹＦＯＲＧ４２２ＭＯＵＳＥＧＬＩＯＢＬＡＳＴＯＭＡＢＹＩＮＴＲＡＴＵＭＯＲＡＬＩＮＪＥＣＴＩＯＮＯＦＲＥＣＯＭＢＩＮＡＮＴＡＤＥＮＯＶＩＲＵＳＥＳ１ＨｏｎｇＢｏ２洪波ＣａｏＸｕｅｔａｏ３曹雪涛Ｙｕ...     

急性脑梗死患者血清瘦素、IL-6水平的变化及意义

目的　通过对6 0例急性脑梗死患者血清瘦素(Leptin)及白细胞介素6 (Interleukine - 6 ;IL - 6 )水平的检测,探讨脑梗塞与瘦素、IL - 6的关系及发生机制。方法　患者6 0例。男37例,女2 3例,年龄39～80岁。均经CT证实。入院后第2天抽取空腹静脉血,用酶联免疫分析法(ELISA)。检测血清瘦素、IL - 6 ,同时检测2 1例健康成人作对照组。结果　脑梗死组瘦素水平显著高于对照组,t=3.99,P <0 .0 1。轻、重症患者无差异。结论　急性脑梗死患者存在高瘦素血症和瘦素抵抗,瘦素参与了能量平衡的调节,瘦素水平增高是急性脑梗死的危险标志物。其发生机理有待深入研究。     

激活骨髓自体移植治疗急性早幼粒细胞白血病

目的　探讨激活骨髓 (ABM)自体移植作为急性早幼粒细胞白血病 (APL)缓解后巩固强化治疗的意义。方法　 31例病人 ,第一次完全缓解 (CR1) 2 7例、CR2 3例、第二次复发部分缓解 (PR) 1例 ;移植预处理方案 :2 7例接受MACC(马法兰、阿糖胞苷、环磷酰胺、环己亚硝脲 )方案 ,5例用TBI +CY(全身放疗 +环磷酰胺 )方案 ;荧光原位杂交测定PML/RARα融合基因 ;用Kaplan Meier生存曲线评估移植后无病生存率 ,COX回归模型分析性别、PML/RARα阳性、移植前状态 (CR1与CR2和PR)、初治时白细胞 (WBC)和血小板 (PBC)值对无病生存的影响。结果　CR1病人移植后无一例复发 ,移植后无病生存期 3～ 113个月、中位无病生存期 4 6个月 ,5年无病生存率为 10 0 % ;CR2病人 1例于移植后 19个月复发 ,另 2例分别无病生存为 7与 4 8个月 ;PR患者在移植后获CR 8个月复发。移植后全部病人均获得造血重建 ,无一例死于移植相关并发症。多因素分析长生存与移植前状态相关 (P <0 .0 5 ) ,而与性别、PML/RARα阳性、初诊时WBC和PBC数无关 ;诱导缓解后PML/RARα阳性与初诊时WBC和PBC数相关。结论　激活骨髓自体移植治疗CR后的APL病人能降低复发率和提高无病生存率、尤是CR1后的APL病人。     

Cytotoxic Activity of Various LAK Cells against Autologous Lung Cancer, K-562 and Daudi Cells

Comparative cytotoxic activity and specificity studies of lymphokineactivated killer (LAK) cells from different sources and preparationswere carried out. Cytotoxic studies of lymphocytes from regionallymph nodes (Rn-LAK), peripheral blood (Pb-LAK) and those stimulatedby autologous tumor cells and then activated by recombinantinterleukine 2 (St-LAK) against autologous lung cancer cells,were conducted using the ⁵¹Cr-releasing test. The cytotoxicactivities of these three LAK cells against autologous fibroblasts,allogeneic tumor cells, K-562 and Daudi cells were also compared.A time course experiment disclosed that the cytotoxic activityof Pb-LAK cells against autologous tumor cells reached a maximumon day 3 and declined shortly after the peak while that of Rn-LAKcells gradually increased to a maximum on day 7 and remainedat a high titer for at least two weeks. The cytotoxic activityof Rn-LAK cells was significantly higher than that of Pb-LAKcells in seven out of 10 individual experiemnts and that ofstimulated LAK (St LAK) cells was higher than the cytotoxicactivities of the other LAK cells in eight out of nine experiments.A specificity study showed that Rn-LAK cells possessed a highercytotoxic activi ty against autologous tumor cells and a lowercytotoxic activity against autologous fibroblasts and allogeneictumor cells than Pb-LAK cells. A comparative study of cytotoxicactivities against K-562, Daudi cells and autologous tumor cellsbetween St- and Rn-LAK cells demonstrated that although therewas no difference in natural killer activity, cytotoxic activityagainst autologous tumor cells as well as the LAK activity ofSt-LAK cells were higher than that of Rn-LAK cells. These resultsindicate that the activities and specificities of LAK cellsdiffer according to their source and preparation.     

La voie IL-2/IL-2R chez la cellule dendritique module à la fois leur synthèse de cytokines et leur capacité à activer des lymphocytes T CD4 allogéniques

The results provide new insights into the role of IL-2/IL-2R pathway in DC. We report that stimulation of human monocyte-derived DC with LPS strongly upregulated CD25 (α chain of the IL-2R) expression. In addition, by using a humanized monoclonal antibody against CD25, we demonstrated that the IL-2 signalling in DC upregulated both IL-12 and γIFN production but decreased IL-10 synthesis. Anti-CD25 treatment reduced the ability of LPS-DC to induce allogeneic CD4⁺ T cell proliferation as compared to LPS-matured DC. In addition, LPS-matured DC treated with IL-2 had a higher allostimulatory capacity compared to LPS-DC. We also found that LPS-matured DC produced IL-2. Thus, IL-2 seems to contribute actively to DC activation through an autocrine pathway. Moreover, IL-2 pathway in DC is involved in T helper priming. These findings might be useful for protocols in cellular therapy and a valuable tool to understand graft rejection versus the acquisition of peripheral tolerance.     

La fièvre récurrente liée au récepteur 1 du TNF (TNF receptor associated periodic syndrome – TRAPS)

Tumour necrosis receptor associated periodic syndrome (TRAPS) is a rare cosmopolitan dominant autosomal disease that belongs to the group of recurrent autoinflammatory syndromes. TRAPS is characterized by recurrent bouts of fever lasting more than 7 days, with arthralgia, myalgia, abdominal pain, erythematous rash and sometimes ocular symptoms. During flares, raised inflammatory markers are constant. The age of onset may occur during childhood but also during adulthood. TRAPS is caused by mutations in the TNF receptor 1 (TNFRSF1A) gene that may occur in most of the populations over the world. In the majority of patients, history shows affected relatives, even if sporadic cases do exist. Management of TRAPS usually involves corticosteroid therapy during inflammatory flares. The most severe cases require a treatment with biological agents (mainly interleukin 1 inhibitors). The prognosis of TRAPS is overall good; the main risk is represented by the development of secondary inflammatory amyloidosis. This risk is greatest in patients with structural mutations leading to conformation abnormalities of the TNFRSF1A receptor. Regular clinical and biological monitoring is essential in the follow-up of TRAPS patients.     

IL-6对血管内皮细胞活性及TF mRNA表达的影响

目的研究IL-6对脐静脉血管内皮细胞（HUVECs）组织因子（TF）的mRNA水平的影响．方法应用胰酶消化HUVECs并进行传代培养,用第二、三代细胞进行试验。测定IL-6（0．5ng／mL）处理前后细胞活性,反转录聚合酶链反应（RT—PCR）法检测细胞内TFmRNA水平。结果72h内,IL-6对HUVECs的活性的影响与正常对照组相比差异无统计学意义。IL-6作用HUVECs6h即诱导TFmRNA表达,12h达到高峰,以后表达减弱,72h不能检测到mRNA;对照组TF mRNA不表达或表达极弱。结论IL-6（0．5ng／mL）对HUVECs的活性不造成直接的影响,同时在24-48h内IL-6（0．5ng／mL）可诱导HUVECs TF表达,这可能与IL-6作为前炎症因子诱导急性炎症反应时相的血液循环障碍相关。