Objective Immune response initiation and regulation require activation of dendritic cells (DCs). However, the mechanism by which ferritin, a carrier for immunogen, induces DCs maturation remains unclear. Results Recombinant ferritin nanoparticle (RFNp), were prepared through the baculovirus expression vector system, formed spherical and hollow cage-liked proteins with a diameter of approximately 12.17 ± 0.87 nm. They induced bone marrow-derived DC (BMDC) maturation via surface molecules up-regulation of (MHC II, CD80, CD86 and CD40), increased pro-inflammatory cytokines production (IL-6, IL-12, TNF-α, and IFN-γ), and decreased antigen capturing capacity. They positively regulated IκBα and NF-κB (p65) phosphorylation, and facilitate NF-κB (p65) translocation into mature BMDCs nuclei. Following pre-treatment of RFNp-treated BMDCs with TLR4 and NF-κB (p65) inhibitors, respectively, surface molecule expression, pro-inflammatory cytokines production, and IκBα and NF-κB (p65) activities were suppressed. RFNp-treated BMDCs can also facilitate T-cell proliferation and differentiation into Th1 and Th2. Conclusion RFNps induced DCs maturation lends the potential application of RFNps as carrier platforms in DC-based vaccine.

中文翻译：

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重组铁蛋白纳米颗粒可通过 TLR4/NF-κB 通路诱导树突细胞成熟

目的免疫反应的启动和调节需要激活树突细胞 (DC)。然而，免疫原载体铁蛋白诱导 DC 成熟的机制尚不清楚。结果重组铁蛋白纳米颗粒(RFNp)，通过杆状病毒表达载体系统制备，形成直径约12.17±0.87 nm的球形和空心笼状蛋白。他们通过表面分子上调（MHC II、CD80、CD86 和 CD40）、增加促炎细胞因子的产生（IL-6、IL-12、TNF-α 和 IFN -γ)，并降低抗原捕获能力。它们正调节 IκBα 和 NF-κB (p65) 磷酸化，并促进 NF-κB (p65) 易位到成熟的 BMDCs 细胞核中。分别用 TLR4 和 NF-κB (p65) 抑制剂预处理 RFNp 处理的 BMDCs 后，表面分子表达、促炎细胞因子的产生以及 IκBα 和 NF-κB (p65) 活性受到抑制。RFNp 处理的 BMDC 还可以促进 T 细胞增殖和分化为 Th1 和 Th2。结论 RFNps 诱导 DCs 成熟有助于 RFNps 作为载体平台在基于 DC 的疫苗中的潜在应用。