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白细胞介素32通过5'-LTR抑制HIV复制 被引量:3

Suppression of HIV Replicaton by Interleukin-32 via 5'-LTR
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摘要 目的:探讨白细胞介素32(IL-32)抑制HIV病毒复制的机制.方法:利用荧光色素酶活性测定筛选抑制HIV复制最显著的IL-32亚型,通过构建HIV的LTR系列截断质粒和TAR茎环结构的系列点突变质粒,确定IL-32抑制HIV复制作用的位点.结果:在Hela、Jurkat、293T三个细胞系中,IL-32γ和IL-32ε两种亚型对HIV的抑制作用最显著.在Hela细胞系中证实IL-32可通过抑制HIV 5'-LTR的活性抑制HIV复制,确定TAR形成的茎环结构在此过程中起重要作用.IL-32与TAR结构相互作用的位点定位在TAR的环状和半环状处.结论:IL-32能抑制HIV复制,可作为HIV治疗的潜在手段. Objective: To investigate the mechanism of interleukin 32(IL-32) inhibition of HIV replication.Methods:The most significant IL-32 subtype of HIV replication was screened by luciferase activity assays.By constructing a series of HIV plasmids containing LTR truncated mutations and point mutations of TAR hairpin,the site of IL-32 inhibition on HIV replication was determined.Results: In the three cell lines of Hela,Jurkat and 293 T,IL-32γ and IL-32ε subtypes had the most significant inhibitory effects on HIV.In Hela cell line,it was confirmed that IL-32 could suppress HIV replication by inhibiting the activity of HIV 5'-LTR,with the hairpin structure formed by TAR playing an important role in this process.The action site of IL-32 interaction with TAR structure was located at the ring and the half ring of TAR.Conclusion: IL-32 can inhibit HIV replication as a potential means of HIV treatment.
出处 《中南民族大学学报(自然科学版)》 CAS 北大核心 2017年第4期40-44,共5页 Journal of South-Central University for Nationalities:Natural Science Edition
基金 国家自然科学基金资助项目(81402668)
关键词 白细胞介素32 人免疫缺陷病毒 长末端重复序列 interleukin-32 ( IL-32) human immunodeficiency virus ( HIV ) long terminal repeat ( LTR )
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  • 1孙冬梅,刘中博,赵岩,宫振伟,李丹,王溪原,曾宪录,刘文广.Runx2参与调控Osterix启动子活性及其基因表达(英文)[J].生物化学与生物物理进展,2006,33(10):957-964. 被引量:21
  • 2Kim SH, Han SY, Azam T, et al. Interleukin-32: a cytokine and inducer of TNF-α[J]. Immunity, 2005, 22( 1 ): 131-142.
  • 3Rasool ST, Tang H, Wu J, et al. Increased level oflL-32 during human immunodeficiency virus infection suppresses HIV replication [J]. Immunol Lett, 2008,117(2 ):161-167.
  • 4Shoda H, Fujio K, Yamaguchi Y, et al. Interactions between IL-32 and tumor necrosis factor alpha contribute to the exacerbation of immune-inflammatory diseases[J]. Arthritis Res Ther, 2006, 8 (6):R166.
  • 5Netea MG, Azam T, Lewis EC, et al. Mycobacterium tuberculosis induces interleukin-32 production through a caspase-1/IL-18/interferon-gamma-dependent mechanism[J]. PLoS Med, 2006,3( 8 ):e277.
  • 6Joosten LA, Netea MG, Kim SH, et al. IL-32, a proinflammatory cy- tokine in rheumatoid arthritis [J]. Proc Natl Acad Sci U S A, 2006, 03( 9 ):3298-3303.
  • 7Netea MG, Lewis EC, Azam T, et al. lnterleukin-32 induces the differentiation of monocytes into maerophage-like cells[J]. Proc Natl Acad Sci U S A, 2008,105(9):3515-3520.
  • 8Kundu M, Basu J. IL-32: an emerging player in the immune response network against tuberculosis[J]. PLoS Med, 2006,3 ( 8 ):e274.
  • 9Netea MG, Azam T, Ferwerda G, et al. IL-32 synergizes with nucleotide oligomerization domain (NOD) 1 and NOD2 ligands for IL- 1 β and IL-6 production through a caspase 1-dependent mechanism [J]. Proc Natl Acad Sci USA, 2005,102:16309-16314.
  • 10Joosten LA, Helsen MM, Saxne T, el al. IL-1αβ, blockade prevents cartilage and bone destruction in murine type Ⅱ collagen-induced arthritis, whereas TNF-α blockade only ameliorates joint inflammation[J]. J Immunol, 1999, 163:5049-5055.

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