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寻常型银屑病患者外周血单个核细胞SOCS-1、SOCS-3 mRNA的表达 被引量：2

The expression of SOCS-1 and SOCS-3 mRNA in patients with psoriasis vulgaris
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摘要 目的:检测细胞因子信号抑制因子SOCS-1、SOCS-3mRNA在寻常型银屑病患者外周血单个核细胞(PBMC)中的表达。方法:从20例银屑病患者及20例健康志愿者外周血中分离PBMC,提取RNA,应用逆转录-聚合酶链反应(RT-PCR)方法检测SOCS-1、SOCS-3mRNA的表达。结果:SOCS-1、SOCS-3mRNA在银屑病患者中表达,在正常人中无表达,活动期银屑病患者较静止期患者SOCS-1、SOCS-3mRNA表达增高。结论:SOCS-1、SOCS-3可能在银屑病的Th1免疫反应中发挥作用。 Objective： To investigate the expressions of SOCS - 1 and SOCS - 3 mRNA in peripheral blood mononuclear cells （PBMCS） of psoriasis vulgaris. Methods： Mononuclear cells in peripheral blood were separated and RNA was abstracted from 20 patients with psoriasis vulgaris and 20 normal controls. Reverse transcription - polymerase chain reaction （ RT - PCR） technique was applied to semi - quantitatively analyze the mRNA expressions. Results： SOCS- 1 and SOCS- 3 mRNA were expressed in all the samples from the patients with psoriasis vulgaris, but not in normal controls. The expression of SOCS - 1 and SOCS - 3 mRNA in patients in progressive stage had a significantly higher level than that in static stage. Conclusion： SOCS - 1 and SOCS - 3 may play an important role in the immune pathogenesisof psoriasis vulgaris.
作者 郭红卫 王京滨 李国明 李顺凡 吴志华
机构地区 广东医学院附属医院皮肤性病研究所 广东省疾病控制中心 广东医学院
出处 《中国麻风皮肤病杂志》 2007年第9期776-778,共3页 China Journal of Leprosy and Skin Diseases
关键词 寻常型银屑病 SOCS-1、SOCS-3 MRNA RT-PCR psoriasis vulgaris mRNA, SOCS- 1, SOCS- 3 RT- PCR
分类号 R758.63 [医药卫生—皮肤病学与性病学]
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参考文献11

  • 1Ghoreschi K,Mrowietz U,Sycemic MR.Therapies for psoriasis inducing interleukin 4 and Th-2 responses.J Mole Med 2003;81(8):471-480.
  • 2Mazzarella G,MacDonald TT,Salvati VM,et al.Constitutive activation of the signal transducer and activator of transcription pathway in celiac disease lesions.Am J Pathol 2003;162(6):1845-1855.
  • 3Yamada S,Shiono S.Control mechanism of JAK/STAT signal transduction pathway.FEBS lett 2003;534(1-3):190-196.
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  • 5Egwuagu CE,Yu CR,Zhang M,et al.Suppressors of cytokine signaling proteins are differentially expressed in Th1 and Th2 cells:Implications for Th cell lineage commitment and maintenance.J Immunol 2002;168(7):3181-3187.
  • 6Dai X,Sayama K,Yamask K,et al.SOCS1-Negative feedback of STAT1 activation is a key pathway in the ds-RNA-induced innate immune response of human keratinocytes.J Invest Dermatol 2006;126:1574-1581.
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同被引文献9

  • 1中华医学会肝病学分会,中华医学会感染病学分会.慢性乙型肝炎防治指南[J].传染病信息,2005,18(z1):1-12. 被引量：467
  • 2Albanesi C, Scarponi C, Sebastiani S, et al. A eytokine-to-cbe mokine axis between T ]ymphocytes and keratinocytes can fa- vor Thl cell accumulation in chronic inflammatory skin disea- ses[J]. J Leukoc Bio1,2001,70(4) :617 623.
  • 3Mascia F,Cataisson C,Lee T C,et al. EGFR regulates the ex- pression of keratinocyte-derived granulocyte/macrophage col ony-stimulating [actor in vitro and in vivo[J]. J Invest Der- matol,2010,130(3) :682-693.
  • 4Federici M,Giustizieri M L,Scarponi C, et al. Impaired IFN- gamma-dependent inflammatory responses in human keratino- cytes overexpressing the suppressor of cytokine signaling 1 [J]. J Immunol,2002,169(1) :434-442.
  • 5Madonna S,Scarpon: C,De Pita' D,et al . Suppressor of cyto- kine signaling I inhibits IFN-gamma inflammatory signaling in human keratinocytes by sustaining ERKI/2 activation[J]. FASEB J,2008,22(9) :3287-3297.
  • 6Yoshimura A, Suzuki M, Sakaguchi R, et al. SOCS,inflamma- tion, and autoirnmunityEJ]. Front Immunol, 2012,3 : 20.
  • 7Van Scott E J, Bonder R H. Interavaginal and interarectal screening of antimitotic drugs for topical effectiveness[J]. J inves Dermatol, 1971,56(2) : 132-139.
  • 8Sakurai H, Tashiro K, Kawabata K, et al. Adenoviral expres- sion of suppressor of cytokine signaling lreduces adenovirus vector-induced innate immune responses[-J]. J Immunol, 2008, 180(7) :4931 4938.
  • 9Whyte C S, Bishop E T, Riickerl D, et al. Suppressor of cyto- kine signaling (SOCS) 1 is a key determinant of differential macrophage activation and function[J]. J Leukoc Biol, 2011, 90(5) : 845-854,.

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中国麻风皮肤病杂志
2007年 第9期

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