Spring (2022-08-31 23:17):
#paper doi: 10.1038/s41590-022-01284-1 Inflammation triggers ILC3 patrolling of the intestinal barrier ① 通过活体成像,观察到小鼠肠道绒毛处的ILC3大多处于几乎不移动的稳定状态;② 利用细菌鞭毛蛋白诱导炎症发生,可增加ILC3的IL-22表达,并增强ILC3的移动能力,ILC3在肠道中的迁移模式也发生显著改变;③ T细胞可抑制ILC3的肠道巡逻行为,而CCR9-CCL25趋化因子信号可增强炎症诱导的ILC3迁移;④ 阻断CCL25介导的ILC3迁移可促进肠道上皮细胞的死亡,从而破坏肠道屏障,ILC3产生的IL-22可抑制肠道上皮细胞的死亡。
IF:27.700Q1 Nature immunology, 2022-09. DOI: 10.1038/s41590-022-01284-1 PMID: 35999393
Inflammation triggers ILC3 patrolling of the intestinal barrier
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Abstract:
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.
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