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干扰素诱导蛋白16在银屑病患者皮损中的表达及其调控 被引量:2

The Research of the Expression and Regulation of IFI16 in Psoriasis Lesions
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摘要 目的研究干扰素诱导蛋白16(interferon inducible protein 16,IFI16)在银屑病中的表达及分布,探讨其在银屑病发病中的作用。方法采用RT-PCR、免疫组化的方法分别检测10例银屑病患者皮损和10例健康人皮肤组织真皮与表皮中IFI16的表达情况;采用RT-PCR、Western印记方法检测IFN-γ,TNF-α,IL-17刺激前后Ha Ca T细胞中IFI16的表达情况。结果银屑病患者皮损处IFI16的表达明显高于健康人皮肤,并且以表皮表达为主,免疫组化结果显示IFI16主要定位于银屑病患者的角质形成细胞中。银屑病相关细胞因子IFN-γ,TNF-α和IL-17可以上调角质形成细胞中IFI16的表达水平。结论IFI16在银屑病患者皮损处表达明显高于正常人皮肤,并且IFN-γ,TNF-α和IL-17可以诱导其表达上调,可能是银屑病角质形成细胞的活化机制之一。 Objective To detect the expression and the location of IFI16 in the lesions of psoriasis patients,and discuss the role of IFI16 in the pathogenesis of psoriasis. Methods RT-PCR and immunohistochemistry technique were used to detect the expression of IFI16 in 10 psoriasis lesion and skin tissue from 10 healthy control. RT-PCR and Western blot were performed to investigate the expression of IFI16 in Ha Ca T cells treated with IFN-γ,TNF-α and IL-17. Results We found that IFI16 expression was increased in psoriasis skin lesions,and was located in the epidermis. RT-PCR and Western blot results showed that psoriasisrelated cytokines IFN-γ,TNF-α and IL-17 could induce the overexpression of IFI16 in Ha Ca T cells( P 〈0. 05). Conclusion IFI16 expression was increased in the psoriasis lesional skin,and could be induced by IFN-γ,TNF-α and IL-17,which might contribute to the activation of keratinocytes.
出处 《中国皮肤性病学杂志》 CAS CSCD 北大核心 2016年第3期239-241,250,共4页 The Chinese Journal of Dermatovenereology
关键词 IFI16 银屑病 角质形成细胞 细胞因子 IFI16 Psoriasis Keratinocytes Cytokines
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  • 1Dawson MJ, Trapani JA. The interferon-inducible autoantigen, IFI 16: localization to the nucleolus and identification of a DNA-binding domain [J]. Biochem Biophys Res Commun, 1995,214 ( 1 ) : 152 - 162.
  • 2Brunette RL, Young JM, Whit!ey DG, et 81. Extensive evolutionary and functional diversity among mammalian AIM2-1ike receptors [J]. J Exp Med,2012,209 ( 11 ) :1969 - 1983.
  • 3Singh VV, Kerur N, Bottero V, et al. Kaposi's sarcoma-associated her- pesvirus latency in endothelial and B cells activates gamma interferon- inducible protein 16-mediated inflammasomes [J]. J Virol, 2013,87 (8) :4417 -4431.
  • 4Kis-Toth K, Szanto A, Thai TH, et al. Cytosolic DNA-activated human dendritic cells are potent activators of the adaptive immune response [J]. J Immuno1,2011,187 (3) : 1222 - 1234.
  • 5Chiliveru S, Rahbek SH, Jensen SK, et al. Inflammatory cytokines break down intrinsic immunological tolerance of human primary kerati- nocytes to cytosolic DNA[J]. J Immunol,2014,192(5) :2395 -2404.
  • 6Nestle FO, Kaplan DH, Barker J. Psoriasis[J]. N Engl J Med,2009, 361 (5) :496 - 509.
  • 7Perera GK, Di Meglio P, Nestle FO. Psoriasis [J]. Annu Rev Pathol, 2012,7:385 -422.
  • 8DellOste V, Gatti D, Giorgio AG, et al. The interferon-inducible DNA- sensor protein IFI16: a key player in the antiviral response[J]. New Microbiol,2015,38( 1 ) :5 -20.
  • 9Orzalli MH, Deluca NA, Knipe DM. Nuclear IFII6 induction of IRF-3 signaling during herpesviral infection and degradation of IFI16 by the viral ICP0 protein[J]. Proc Natl Acad Sci USA,2012,109(d4) :E3008- E3017.
  • 10Caneparo V, Cena T, De Andrea M, et al. Anti-IFll6 antibodies and their relation to disease characteristics in systemic lupus erythematosus [J]. Lupus,2013,22(6) :607 -613.

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