Microbial exposure during early life has persistent effects on natural killer T cell function.
Microbial exposure during early life has persistent effects on natural killer T cell function.
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DOI：
10.1126/science.1219328
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发表时间：
2012-04-27
期刊：
影响因子：
--
通讯作者：
Blumberg RS
中科院分区：
文献类型：
--
作者：
Olszak T;An D;Zeissig S;Vera MP;Richter J;Franke A;Glickman JN;Siebert R;Baron RM;Kasper DL;Blumberg RS
儿童早期接触微生物与免疫介导的疾病如炎症性肠病（IBD）和哮喘的保护有关。在这里，我们表明，在无菌（GF）小鼠，不变的自然杀伤T（iNKT）细胞积累在结肠固有层和肺，导致IBD和过敏性哮喘模型的发病率增加相比，特定的病原体-无小鼠。这与肠和肺趋化因子配体CXCL 16的表达增加有关，CXCL 16与粘膜iNKT细胞增加有关。用常规微生物群定殖幼年而非成年GF小鼠保护动物免于粘膜iNKT积累和相关病理。这些结果表明，与肠道微生物的年龄敏感性接触对于建立粘膜iNKT细胞对随后环境暴露的耐受性至关重要。
Exposure to microbes during early childhood is associated with protection from immune-mediated diseases such as inflammatory bowel disease (IBD) and asthma. Here, we show that in germ-free (GF) mice, invariant natural killer T (iNKT) cells accumulate in the colonic lamina propria and lung, resulting in increased morbidity in models of IBD and allergic asthma as compared with that of specific pathogen-free mice. This was associated with increased intestinal and pulmonary expression of the chemokine ligand CXCL16, which was associated with increased mucosal iNKT cells. Colonization of neonatal—but not adult—GF mice with a conventional microbiota protected the animals from mucosal iNKT accumulation and related pathology. These results indicate that age-sensitive contact with commensal microbes is critical for establishing mucosal iNKT cell tolerance to later environmental exposures.
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