A dedicated promoter drives constitutive expression of the cell-autonomous immune resistance GTPase, Irga6 (IIGP1) in mouse liver.

A dedicated promoter drives constitutive expression of the cell-autonomous immune resistance GTPase, Irga6 (IIGP1) in mouse liver.
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DOI:
10.1371/journal.pone.0006787
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发表时间:
2009-08-26
期刊:
影响因子:
3.7
通讯作者:
Howard JC
Howard JC
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Zeng J;Parvanova IA;Howard JC

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一般来说,免疫效应分子是由感染诱导的。然而,在小鼠肝脏中发现了细胞自主抗性GTP酶IrGa6(IIGP1)的强结构性表达,而以往的证据表明该蛋白的表达完全依赖于干扰素γ的诱导。在肝脏中,IrGa6的组成性和干扰素γ诱导的表达依赖于两个独立的未翻译的5‘外显子的转录,这两个外显子交替地拼接到编码全长蛋白序列的长外显子中。IrGa6在新鲜分离的肝细胞中组成性表达,并在这些细胞中聚集在感染弓形虫速殖子的寄生液泡膜上。文中还讨论了IRGA6的结构性肝细胞表达在抵抗肠道寄生虫通过肝脏门脉系统侵袭中的作用。
In general, immune effector molecules are induced by infection. However, strong constitutive expression of the cell-autonomous resistance GTPase, Irga6 (IIGP1), was found in mouse liver, contrasting with previous evidence that expression of this protein is exclusively dependent on induction by IFNγ. Constitutive and IFNγ-inducible expression of Irga6 in the liver were shown to be dependent on transcription initiated from two independent untranslated 5′ exons, which splice alternatively into the long exon encoding the full-length protein sequence. Irga6 is expressed constitutively in freshly isolated hepatocytes and is competent in these cells to accumulate on the parasitophorous vacuole membrane of infecting Toxoplasma gondii tachyzoites. The role of constitutive hepatocyte expression of Irga6 in resistance to parasites invading from the gut via the hepatic portal system is discussed.
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