Retinoic Acid Differentially Regulates the Migration of Innate Lymphoid Cell Subsets to the Gut.
Retinoic Acid Differentially Regulates the Migration of Innate Lymphoid Cell Subsets to the Gut.
复制标题
视黄酸差异调节先天淋巴细胞亚群向肠道的迁移。
DOI：
10.1016/j.immuni.2015.06.009
复制
发表时间：
2015-07-21
期刊：
影响因子：
32.4
通讯作者：
Kim CH
中科院分区：
文献类型：
--
作者：
Kim MH;Taparowsky EJ;Kim CH
不同的先天性淋巴样细胞（ILC）如ILC1，ILC2和ILC3分布在肠道中，但这些ILC如何为该器官发展组织向性尚不清楚。我们报告说，在迁移到肠道ILC首先经历了一个“开关”在他们的归巢受体的表达从淋巴到肠道归巢受体。这一过程受到粘膜树突状细胞和肠道特异性组织因子维甲酸（RA）的调节。归巢受体的这种变化是肠内ILC的长期群体和效应功能所必需的。只有ILC1和ILC3，而不是ILC2，在肠道相关淋巴组织中进行RA依赖性归巢受体转换。相反，ILC2在骨髓中发育期间以很大程度上不依赖RA的方式获得肠道归巢受体，并且可以直接迁移到肠道。因此，不同的程序调节ILC亚群向肠的迁移以调节先天免疫。
Distinct groups of innate lymphoid cells (ILCs) such as ILC1, ILC2 and ILC3 populate the intestine, but how these ILCs develop tissue tropism for this organ is unclear. We report that prior to migration to the intestine ILCs first undergo a `switch' in their expression of homing receptors from lymphoid to gut homing receptors. This process is regulated by mucosal dendritic cells and the gut-specific tissue factor retinoic acid (RA). This change in homing receptors is required for long-term population and effector function of ILCs in the intestine. Only ILC1 and ILC3, but not ILC2, undergo the RA-dependent homing receptor switch in gut-associated lymphoid tissues. In contrast, ILC2 acquire gut homing receptors in a largely RA-independent manner during their development in the bone marrow and can migrate directly to the intestine. Thus, distinct programs regulate the migration of ILC subsets to the intestine for regulation of innate immunity.