Cousins R J, Lanningham-Foster L
Food Science and Human Nutrition Department, Center for Nutritional Sciences, University of Florida, Gainesville, FL 32611-0370, USA.
J Infect Dis. 2000 Sep;182 Suppl 1:S81-4. doi: 10.1086/315917.
Cysteine-rich intestinal protein (CRIP), a member of the LIM protein family, has a unique double zinc finger motif as the defining feature. CRIP is highly expressed in intestine and immune cells. CRIP 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 CRIP 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.
富含半胱氨酸的肠道蛋白（CRIP）是LIM蛋白家族的成员，具有独特的双锌指基序作为其特征。CRIP在肠道和免疫细胞中高度表达。用脂多糖（LPS）对CRIP转基因（Tg）小鼠和非转基因对照进行攻击。LPS给药后，Tg小鼠血清中γ干扰素和肿瘤坏死因子-α的浓度较低，而白细胞介素-6和-10的浓度较高。过表达CRIP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一致，这种调节作用会导致Th1和Th2细胞因子失衡。在金属硫蛋白基因敲除小鼠中，LPS对CRIP蛋白水平的刺激作用消失，这表明金属硫蛋白是这种锌指蛋白的锌来源，并且进一步表明这可能反映了与锌营养状况以及锌缺乏时观察到的异常Th1/Th2细胞因子平衡之间的关系。
