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A new marine-derived sulfoglycolipid triggers dendritic cell activation and immune adjuvant response

机译:一种新的海洋来源的磺基糖脂触发树突状细胞激活和免疫佐剂反应

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摘要

Dendritic Cells (DCs) recognize infectious non-self molecules and engage the adaptive immune system thereby initiating long lasting, antigen-specific responses. As such, the ability to activate DCs is considered a key tool to enhance the efficacy and quality of vaccination. Here we report a novel immunomodulatory sulfolipid named β-SQDG18 that prototypes a class of natural-derived glycolipids able to prime human DCs by a TLR2/TLR4-independent mechanism and trigger an efficient immune response in vivo. β-SQDG18 induces maturation of DC with the upregulation of MHC II molecules and co-stimulatory proteins (CD83, CD86), as well as pro-inflammatory cytokines (IL-12 and INF-γ). Mice immunized with OVA associated to β-SQDG18 (1:500) produced a titer of anti-OVA Ig comparable to traditional adjuvants. In an experimental model of melanoma, vaccination of C57BL/6 mice with β-SQDG18-adjuvanted hgp10 peptide elicited a protective response with a reduction in tumour growth and increase in survival.
机译:树突状细胞(DC)识别感染性非自身分子并参与适应性免疫系统,从而引发持久的抗原特异性反应。这样,激活DC的能力被认为是增强疫苗接种效力和质量的关键工具。在这里,我们报告了一种新型的称为β-SQDG18的免疫调节硫脂,其原型为一类天然来源的糖脂,能够通过不依赖TLR2 / TLR4的机制引发人DC并触发体内有效的免疫应答。 β-SQDG18通过上调MHC II分子和共刺激蛋白(CD83,CD86)以及促炎性细胞因子(IL-12和INF-γ)诱导DC成熟。用与β-SQDG18相关的OVA免疫的小鼠(1:500)可产生与传统佐剂相当的抗OVA Ig效价。在黑色素瘤的实验模型中,用β-SQDG18佐剂的hgp10肽对C57BL / 6小鼠进行疫苗接种可引起保护性反应,从而减少肿瘤的生长并增加存活率。

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