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Inflammation triggers ILC3 patrolling of the intestinal barrier
Nature Immunology ( IF 27.7 ) Pub Date : 2022-08-23 , DOI: 10.1038/s41590-022-01284-1
Angélique Jarade 1 , Zacarias Garcia 2 , Solenne Marie 1 , Abdi Demera 3 , Immo Prinz 3 , Philippe Bousso 2 , James P Di Santo 1 , Nicolas Serafini 1
Affiliation  

An orchestrated cellular network, including adaptive lymphocytes and group 3 innate lymphoid cells (ILC3s), maintains intestinal barrier integrity and homeostasis. T cells can monitor environmental insults through constitutive circulation, scanning tissues and forming immunological contacts, a process named immunosurveillance. In contrast, the dynamics of intestinal ILC3s are unknown. Using intravital imaging, we observed that villus ILC3s were largely immotile at steady state but acquired migratory ‘patrolling’ attributes and enhanced cytokine expression in response to inflammation. We showed that T cells, the chemokine CCL25 and bacterial ligands regulated intestinal ILC3 behavior and that loss of patrolling behavior by interleukin-22 (IL-22)-producing ILC3s altered the intestinal barrier through increased epithelial cell death. Collectively, we identified notable differences between the behavior of ILC3s and T cells, with a prominent adaptation of intestinal ILC3s toward mucosal immunosurveillance after inflammation.



中文翻译:

炎症触发肠屏障的 ILC3 巡逻

一个协调的细胞网络,包括适应性淋巴细胞和第 3 组先天淋巴细胞 (ILC3),可维持肠道屏障的完整性和体内平衡。T 细胞可以通过组成循环、扫描组织和形成免疫接触来监测环境损害,这一过程称为免疫监视。相比之下,肠道 ILC3 的动力学是未知的。使用活体成像,我们观察到绒毛 ILC3 在稳定状态下基本上是不动的,但获得了迁移的“巡逻”属性,并增强了对炎症反应的细胞因子表达。我们发现 T 细胞、趋化因子 CCL25 和细菌配体调节肠道 ILC3 行为,并且产生白细胞介素 22 (IL-22) 的 ILC3 丧失巡逻行为通过增加上皮细胞死亡来改变肠道屏障。集体,

更新日期:2022-08-24
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