IGIF does not drive Th1 development but synergizes with IL-12 for interferon-gamma production and activates IRAK and NF kappa B
IGIF does not drive Th1 development but synergizes with IL-12 for interferon-gamma production and activates IRAK and NF kappa B
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DOI：
10.1016/s1074-7613(00)80378-7
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发表时间：
1997-10-01
期刊：
影响因子：
32.4
通讯作者：
OGarra, A
中科院分区：
文献类型：
--
作者：
Robinson, D;Shibuya, K;OGarra, A
在这些研究中，IFN γ诱导因子（IGIF）与IL-12不同，在BALB/c或C57Bl/6小鼠中不驱动Th1的发展，但与IL-1 α一样，在BALB/c小鼠中增强了IL-12驱动的Th1的发展。IGIF和IL-12协同Th1细胞产生IFN γ。与IL-1不同，IGIF对Th2细胞没有影响。IGIF通过IL-1受体相关激酶IRAK信号传导，诱导Th1细胞中p65/p50 NFB的核易位。IL-1 α对Th1细胞的增殖、细胞因子产生或NFKB激活没有影响，但对Th2细胞的NFKB和增殖有激活作用。因此，Th1和Th2细胞对IL-1家族分子的反应性和受体表达可能不同。IGIF和IL-1 α可能分别不同地放大Th1和Th2效应反应。
In these studies, IFN gamma-inducing factor (IGIF), unlike IL-12, did not drive Th1 development in BALB/c or C57Bl/6 mice, but like IL-1 alpha, potentiated IL-12-driven Th1 development in BALB/c mice. IGIF and IL-12 synergized for IFN gamma production from Th1 cells. Unlike IL-1 alpha, IGIF had no effect on Th2 cells. IGIF signaled through IRAK, IL-1 receptor-associated kinase, to induce nuclear translocation of p65/p50 NFB in Th1 cells. IL-1 alpha had no effect on proliferation, cytokine production, or NFKB activation in Th1 cells but activated NFKB and proliferation in Th2 cells. Thus, Th1 and Th2 cells may differ in responsiveness and receptor expression for IL-1 family molecules. IGIF and IL-1 alpha may differentially amplify Th1 and Th2 effector responses, respectively.