Xin Xiaofei, Zhou Yong, Lyu Yifu, Zhu Ying, Wu Di, Li Jingjing, Qin Chao, Yin Lifang
Department of Pharmaceutics, China Pharmaceutical University, Nanjing, China.
Department of Pharmaceutics, China Pharmaceutical University, Nanjing, China.
J Control Release. 2023 Oct 28. doi: 10.1016/j.jconrel.2023.10.035.
Psoriatic self-antigen LL37 has the ability to stimulate skin-homing T lymphocytes, which is the constitutive factor for the relapse of psoriasis. The local inflammatory modulation in psoriatic skin is not sufficient for the restoration of immune homeostasis. In this study, we found the expression levels of disease specific proteins including LL37, S100A8 and S100A9 were significantly increased in psoriasis. The self-assembled nanoparticles based on methoxy-poly(ethylene glycol)-block-poly(L-histidine) and methoxy-poly(ethylene glycol)-block-poly(L-lactic acid) (HLNPs) were capable of interacting and absorbing these disease specific proteins, leading to the accumulation of HLNPs in peripheral inflammatory immune cells. Therefore, we proposed an "Antigen-scavenging" polypeptide nano-system assembled from the "sandwich" structure composed of HLNPs, siRNA-TNFα, and oligolysine conjugated methotrexate prodrug (HLNP-MNs), with the encapsulation of ROS-responsive methotrexate prodrug and siRNA-TNFα. We evaluated the biological fate of HLNP-MNs in vivo, the ROS-responsive release of methotrexate (MTX) and siRNA-TNFα in inflammatory immune cells, the suppression of immune response triggered by autoantigen LL37 and the inhibition of skin-homing T lymphocytes from the aspects of "nanoparticle-protein" interaction, cellular level and mouse models. The design of "Antigen-scavenging" polypeptide nanoparticles with loading of MTX and siRNA-TNFα, can shed light on restoring immune homeostasis in psoriasis.
银屑病自身抗原LL37具有刺激皮肤归巢性T淋巴细胞的能力,这是银屑病复发的构成因素。银屑病皮肤中的局部炎症调节不足以恢复免疫稳态。在本研究中,我们发现包括LL37、S100A8和S100A9在内的疾病特异性蛋白在银屑病中的表达水平显著升高。基于甲氧基聚(乙二醇)-嵌段-聚(L-组氨酸)和甲氧基聚(乙二醇)-嵌段-聚(L-乳酸)(HLNPs)自组装的纳米颗粒能够与这些疾病特异性蛋白相互作用并吸收它们,导致HLNPs在外周炎症免疫细胞中积累。因此,我们提出了一种由HLNPs、siRNA-TNFα和寡聚赖氨酸共轭甲氨蝶呤前药(HLNP-MNs)组成的“三明治”结构组装而成的“抗原清除”多肽纳米系统,其中封装了ROS响应性甲氨蝶呤前药和siRNA-TNFα。我们从“纳米颗粒-蛋白质”相互作用、细胞水平和小鼠模型等方面评估了HLNP-MNs在体内的生物学命运、炎症免疫细胞中甲氨蝶呤(MTX)和siRNA-TNFα的ROS响应性释放、自身抗原LL37触发的免疫反应的抑制以及皮肤归巢性T淋巴细胞的抑制。负载MTX和siRNA-TNFα的“抗原清除”多肽纳米颗粒的设计,可为恢复银屑病中的免疫稳态提供思路。