目的 探讨在小鼠树突状细胞（DC）成熟过程中核因子-kB（NF-kB）基因的作用。方法 应用特异性NF-kB寡聚脱氧核甘酸诱骗剂（NF-kBODNDecoys）阻断NF-kB活性，观察DC形态、细胞表面分子表达以及同种T淋巴细胞增殖反应的变化，了解NF-kB其因对DC成熟及免疫生物活性的影响。结果 NF-kBODNDecoys的有效摄取，抑制了DC表面共刺激分子CD80、CD86、CD40的表达和白细胞介素12（IL-12）的分泌，阻碍了DC的发育成熟，这种阻碍作用不可被脂多糖（LPS）所逆转。混合淋巴细胞反应显示，NF-kBODNDecoys的应用可诱导DC刺激同种T淋巴细胞低反应活性，抑制了T细胞IL-2和y-十扰素（IFN-y）的分泌。结论 NF-kB是DC发育成熟过程中关键性调控基因。应用NF-KbODNDecoys可抑制DC的成熟，从而为生成耐受原性未成熟DC、诱导移植免疫耐受提供了一种新的途径。

We investigated whether recipient dendritic cells (DCs), pretreated with nuclear factor-kB oligodeoxyribonucleotide decoy (NF-kB ODN decoy) and loaded with ultraviolet B-irradiated donor apoptotic splenocytes (Apo-SCs), were able to induce murine cardiac allograft tolerance. Heterotopic vascularized heart transplantation was performed from BALB/c to C57BL/6 mice, and recipients (C57BL/6) were given one injection of recipient DCs pretreated with NF-kB ODN decoy and loaded with donor (BALB/c) apoptotic SCs (decoy Apo-SCs DCs) through the portal vein at 7 days, before heart transplantation in the absence of immunosuppression. The cardiac allograft survival time and the expressive levels of intragraft cytokine genes [interleukin (IL)-2, IL-10, and interferon-γ] were evaluated. Our results indicated that injection of decoy Apo-SCs DCs significantly prolonged vascularized heart allograft survival and led to skewing of intragraft cytokine expression towards T helper 2 (IL-10). The mechanisms can be useful for therapy of allograft rejection with minimization of systemic immunosuppression.

目的 观察肝大部切除大鼠再生血清和肝细胞生长因子（HGF）诱导骨髓干细胞向肝实质细胞分化的作用；探讨骨髓干细胞向肝细胞分化和增殖的体外培养条件和方法，为患者应用自身骨髓细胞修复损伤肝脏提供实验依据。方法 制作肝大部切除大鼠肝再生动物模型，收集术后24h血清；分别应用鼠肝再生血清和HGF对大鼠骨髓细胞进行定向诱导分化培养；以免疫组化、RT-PCR和westernblot等方法对分化不同阶段细胞进行检测。将分化细胞经尾静脉输入同系大鼠，观察输注细胞在肝、脾内的生长情况。结果 活体移植分化细胞能定向迁移至肝和脾；体外及体内分化细胞在mRNA水平和蛋白贡水平均表达白蛋白，并在一定时期内表达甲胎蛋白。结论 大鼠骨髓干细胞在肝大部切除再生血清或HGF的诱导下能横向分化为肝实质样细胞。