Arrunategui-Correa Victor, Kim Hyun Sil
Division of Gastroenterology, Department of Medicine, University of California, San Diego, School of Medicine, La Jolla, CA, USA.
Cell Immunol. 2004 Feb;227(2):109-20. doi: 10.1016/j.cellimm.2004.02.003.
To address the role of CD1d in mucosal immune regulation in bacterial infection, we infected CD1d KO mice with Listeria monocytogenes (Lm). A higher systemic bacterial burden associated with inflammatory lymphocytic infiltrations within the intestine was found in CD1d KO compared with wild type (WT) mice. Lm induced strong IFN-gamma mRNA expression in the liver of WT and the intestine of CD1d KO mice, thus demonstrating the dual, opposing immune activities of IFN-gamma in Lm infection that is dependent on CD1d and/or NKT cells. Analysis of hepatic T cell population demonstrated a reduction of NK1.1(+)TCRbeta+ cells in both mice, followed by recovery only in WT mice. Last, the proportion of alpha4beta1 integrin on lung lymphocytes from CD1d KO was dramatically increased compared with WT mice. Thus, the absence of CD1d resulted in increased susceptibility towards Listeria infection, induced changes in NKT cells, and increased trafficking of alpha4beta1 molecule to inflamed lung.
为了研究CD1d在细菌感染的黏膜免疫调节中的作用，我们用单核细胞增生李斯特菌（Lm）感染了CD1d基因敲除（KO）小鼠。与野生型（WT）小鼠相比，在CD1d KO小鼠中发现与肠道内炎性淋巴细胞浸润相关的全身细菌载量更高。Lm在WT小鼠的肝脏和CD1d KO小鼠的肠道中诱导强烈的干扰素-γ（IFN-γ）mRNA表达，从而证明IFN-γ在依赖于CD1d和/或自然杀伤T（NKT）细胞的Lm感染中具有双重、相反的免疫活性。对肝脏T细胞群体的分析表明，两种小鼠中NK1.1(+)TCRβ+细胞均减少，随后仅在WT小鼠中恢复。最后，与WT小鼠相比，CD1d KO小鼠肺淋巴细胞上α4β1整合素的比例显著增加。因此，CD1d的缺失导致对李斯特菌感染的易感性增加，诱导NKT细胞发生变化，并增加α4β1分子向炎症肺部的迁移。
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