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粉尘螨通过调节树突状细胞功能促进卵清蛋白诱导的气道过敏反应。

Pplase of Dermatophagoides farinae promotes ovalbumin-induced airway allergy by modulating the functions of dendritic cells in a mouse model.

机构信息

State Key Laboratory of Respiratory Disease for Allergy at Shenzhen University, Shenzhen Key Laboratory of Allergy &Immunology, Shenzhen University School of Medicine, Shenzhen, China.

Shenzhen ENT Institute, Longgang ENT Hospital, Shenzhen, China.

出版信息

Sci Rep. 2017 Feb 27;7:43322. doi: 10.1038/srep43322.

Abstract

Our previous studies revealed that many proteins in addition to the known allergens of D. farinae have not been fully characterized. We observed that Pplase did not respond to serum collected from patients sensitized to D. farinae. In a mouse model, Pplase significantly enhanced airway hyperresponsiveness (AHR) and Th2 responses induced by ovalbumin (OVA) compared with mice treated with OVA alone. Moreover, exposure to Pplase significantly increased the expression of IRF4, CD80, CD83, MHCII and TNF-α in DC2.4 cells, which was abolished in the presence of a TLR4 inhibitor. In vitro T cell polarization experiments revealed that Pplase alone could not induce T cell polarization but enhanced T cell polarization together with OVA. In addition, transfer of Pplase-primed bone marrow-derived DCs (BMDCs) to naïve mice enhanced AHR and Th2 immune responses in mice sensitized to OVA. In conclusion, Pplase is not an allergen of D. farinae but can activate DC cells to facilitate OVA-induced allergic responses.

摘要

我们之前的研究表明,除了已知的屋尘螨过敏原外,还有许多蛋白质尚未得到充分的表征。我们观察到,Pplase 对屋尘螨过敏患者的血清没有反应。在小鼠模型中,与单独用 OVA 处理的小鼠相比,Pplase 显著增强了由卵清蛋白(OVA)诱导的气道高反应性(AHR)和 Th2 反应。此外,暴露于 Pplase 可显著增加 DC2.4 细胞中 IRF4、CD80、CD83、MHCII 和 TNF-α的表达,而 TLR4 抑制剂的存在则消除了这种表达。体外 T 细胞极化实验表明,Pplase 本身不能诱导 T 细胞极化,但可与 OVA 一起增强 T 细胞极化。此外,将 Pplase 预激活的骨髓来源的树突状细胞(BMDCs)转移至对 OVA 致敏的小鼠中,可增强小鼠的 AHR 和 Th2 免疫反应。总之,Pplase 不是屋尘螨的过敏原,但可激活 DC 细胞,促进 OVA 诱导的过敏反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4090/5327411/205d6f4df886/srep43322-f1.jpg

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