中文摘要：

目的观察热休克蛋白60（HSP60）对小鼠骨髓树突状细胞（dendritic cell,DC）生物学活性的影响,并探讨核因子κB必需分子（NF-κB essential modulator,NEMO）结合的小分子多肽（NEMO binding domain,NBD）对DC活性的干预作用,为NBD多肽的临床应用提供理论依据。方法培养小鼠骨髓源性DC,分为对照组、HSP60组及NBD组,对照组在正常条件下培养,HSP60组加入终质量浓度为10μg/ml的HSP60,NBD组在加入NBD（50μmol/ml）4 h后给予10μg/ml的HSP60刺激,继续培养3 d。流式细胞术检测DC细胞表面CD80、CD86及MHC-Ⅱ分子的变化,ELISA法检测各组DC分泌肿瘤坏死因子-α（TNF-α）、干扰素-γ（IFN-γ）和白介素-12（IL-12）的质量浓度,免疫细胞化学检测DC核因子-κB（NF-κB）的表达,混合淋巴细胞培养检测T细胞增殖能力。结果 HSP60可促进DC高表达CD80、CD86及MHC-Ⅱ分子,促进Th1型细胞因子TNF-α、IFN-γ及IL-12释放、NF-κB高表达并易位于核内,并诱导T细胞增殖,NBD多肽可阻断HSP60的这些效应。结论 NBD多肽可抑制HSP60诱导的DC激活。

英文摘要：

To explore the impact of HSP60 on biological activity of dendritic cells（DCs） cultured from murine bone marrow, and to evaluate the intervention effect of NF-κB essential modifier binding domain（NBD） peptide on activation of the DCs, mouse DCs were generated from bone marrow cells and were divided into control group,HSP60 group and NBD group. DCs in control group was cultured with normal condition, while HSP60 group was added with HSP60 of the final concentrations of 10 μg/ml. NBD peptide（50 μmol/ml） was added in NBD group, and4 hours later HSP60 of the final concentrations of 10 μg/ml was added. All groups were continuously cultured for3 days. Then the CD80, CD86 and MHC- Ⅱ were detected by flow cytometry; ELISA was used to detect the concentration of TNF-α, IFN-γ and IL-12 in the supernatant; mixed lymphocyte reaction（MLR） was used to detect the function properties of DCs; and immunochemistry was used to detect the concentration of MyD88 and NF-κB.The results showed that HSP60 stimulation increased the expressions of CD80, CD86 and MHC- Ⅱ in the cytomembrane of DCs, and elevated TNF-α, IFN-γ, IL-12 concentration in the supernatant. HSP60 stimulation also increased the NF-κB expression and shift the expression to karyon. NBD peptide could inhibit these effects of HSP60. Thus, we concluded that NBD peptide can suppress the maturation of DCs induced by HSP60.