中国麻风皮肤病杂志 ›› 2017, Vol. 33 ›› Issue (7): 398-402.

• 论著 • 上一篇    下一篇

重组Ad-SOCS1介导的树突状细胞源外泌体对银屑病样小鼠模型的影响

曾凡杞 冉灵芝 胡鹏飞 刘鹄荫   

  1. 深圳市光明新区人民医院皮肤科，深圳，518106
  • 出版日期:2017-07-15 发布日期:2018-12-01
  • 通讯作者: 曾凡杞，E-mail：zeng-2005@126.com

Effects of Ad-SOCS1 infected DCs-secreted exosome on the therapy of psoriasis-like murine models

Zeng Fanqi, Ran Linzhi, Hu Pengfei, Liu Huying.   

  1. Shenzhen Guangming New District People’s Hospital, Shenzhen, 518106
  • Online:2017-07-15 Published:2018-12-01
  • Contact: ZENG Fanqi, E-mail：zeng-2005@126.com

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摘要： 目的：明确重组腺病毒(Ad-SOCS1)介导的树突状细胞（DCs）分泌的外泌体对银屑病样小鼠模型的影响。方法：Ad-SOCS1腺病毒感染小鼠骨髓来源的DCs，分离纯化培养物中的外泌体，Western Blot分析鉴定外泌体中的CD63、SOCS1和ICAM-1蛋白。。咪喹莫特（IMQ）诱导10只银屑病样小鼠模型，其中5只给予外分泌体治疗（外分泌体组）组，5只作为对照（IMQ组）。RT-PCR检测小鼠外周血IL-17A、IL-22和IL-23 mRNA的表达水平。结果：外泌体中能够鉴定到SOCS1、CD63和ICAM-1蛋白。外分泌体组小鼠的银屑病样表现?较IMQ组轻。外分泌体组小鼠外周血IL-17A和IL-23 mRNA的表达低于IMQ组（P <0.01），IL-22水平两组间无显著差异（P >0.05）。结论：Ad-SOCS1感染DC后培养物分离的外泌体可改善银屑病的症状，其机制可能与外泌体SOCS1抑制IL-17A有关。

关键词: SOCS1, 银屑病, 树突状细胞, 外泌体, IL-17A

Abstract: Objective: To determine the effect of exosome derived from the dendritic cells (DCs) induced by Adenovirus-Suppressor of cytokine signaling1 (Ad-SOCS1) on the psoriasis-like murine models. Methods: The exosomes of murine DCs were infected by Ad-SOCS1. The levels of SOCS1, CD63 and ICAM-1 from exosome were detected by Western Blot. The psoriasis-like murine models were induced by imiquimod (IMQ) and were divided into the DC-exo(s) group and IMQ-group. The mRNA levels of IL-17A, IL-22 and IL-23 in peripheral blood were detected by RT-PCR. Results: SOCS1, ICAM-1 and CD63 proteins in exosomes were detected. The symptoms??of?the psoriasis-like mouse in the?DC-exo(s) group?were better than?that in the control?group. The level of IL-17A and IL-23 mRNA were higher in the DC-exo-S group than that in the control group. There was no significant difference in the IL-22 level between the DC-exo-S group and control group. Conclusions: Exosome from Ad-SOCS1-infected DCs culture can improve the psoriasis-like murine models. The mechanisms may be associated with the inhibition of IL-17A and IL-23. 

Key words: suppressor of cytokine signaling1 (SOCS1), psoriasis, dendritic cells (DCs), exosome, IL-17A