Regulation of cysteine-rich intestinal protein, a zinc finger protein, by mediators of the immune response
Regulation of cysteine-rich intestinal protein, a zinc finger protein, by mediators of the immune response
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DOI：
10.1086/315917
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发表时间：
2000-09-01
影响因子：
6.4
通讯作者：
Lanningham-Foster, L
中科院分区：
文献类型：
--
作者：
Cousins, RJ;Lanningham-Foster, L
富含半胱氨酸的肠道蛋白(CRIP)是LIM蛋白家族的一员，具有独特的双锌指基序。GRIP在肠道和免疫细胞中高度表达。用脂多糖(LPS)攻击GRIP转基因(TG)小鼠和非转基因对照小鼠后，血清中干扰素-γ和肿瘤坏死因子-α的浓度降低，而IL-6和-10的浓度升高。CRIP过表达的脾细胞产生相同的细胞因子谱。这些反应与该蛋白在细胞分化中的调节作用是一致的，细胞分化产生Th1和Th2细胞因子的失衡。在金属硫蛋白基因敲除小鼠中，消除了脂多糖对GRIP蛋白水平的刺激，这表明金属硫蛋白是该锌指蛋白的锌来源，并进一步反映了这可能与锌营养状况和锌缺乏时观察到的Th1/Th2细胞因子异常平衡有关。
Cysteine-rich intestinal protein (CRIP), a member of the LIM protein family, has a unique double zinc finger motif as the defining feature. GRIP is highly expressed in intestine and immune cells. GRIP transgenic (Tg) mice and nontransgenic controls were challenged with lipopolysaccharide (LPS), Serum concentrations of interferon-gamma and tumor necrosis factor-alpha were less while those of interleukin-6 and -10 were greater in the Tg mice following LPS administration. CRIP-overexpressing splenocytes produce the same cytokine profile. These responses are consistent with a regulatory role for this protein in cell differentiation, which produces an imbalance in Th1 and Th2 cytokines. Stimulation of GRIP protein levels by LPS is eliminated in metallothionein knockout mice, suggesting metallothionein is the source of zinc for this zinc finger protein and, further, that this could reflect a relationship to the zinc nutritional status and to the aberrant Th1/Th2 cytokine balance observed in zinc deficiency.