生物
先天性淋巴细胞
细胞生物学
先天免疫系统
免疫系统
共生
白细胞介素22
免疫学
细菌
趋化因子
微生物学
细胞因子
白细胞介素
遗传学
作者
Tetsuro Kobayashi,Benjamin Voisin,Doyoung Kim,Elizabeth A. Kennedy,Jay‐Hyun Jo,Han-Yu Shih,Amanda Truong,Thomas Doebel,Keiko Sakamoto,Chang‐Yi Cui,David Schlessinger,Kazuyo Moro,Susumu Nakae,Keisuke Horiuchi,Jinfang Zhu,Warren J. Leonard,Heidi H. Kong,Keisuke Nagao
出处
期刊:Cell
[Elsevier]
日期:2019-02-01
卷期号:176 (5): 982-997.e16
被引量:151
标识
DOI:10.1016/j.cell.2018.12.031
摘要
Immune cells and epithelium form sophisticated barrier systems in symbiotic relationships with microbiota. Evidence suggests that immune cells can sense microbes through intact barriers, but regulation of microbial commensalism remain largely unexplored. Here, we uncovered spatial compartmentalization of skin-resident innate lymphoid cells (ILCs) and modulation of sebaceous glands by a subset of RORγt+ ILCs residing within hair follicles in close proximity to sebaceous glands. Their persistence in skin required IL-7 and thymic stromal lymphopoietin, and localization was dependent on the chemokine receptor CCR6. ILC subsets expressed TNF receptor ligands, which limited sebocyte growth by repressing Notch signaling pathway. Consequently, loss of ILCs resulted in sebaceous hyperplasia with increased production of antimicrobial lipids and restricted commensalism of Gram-positive bacterial communities. Thus, epithelia-derived signals maintain skin-resident ILCs that regulate microbial commensalism through sebaceous gland-mediated tuning of the barrier surface, highlighting an immune-epithelia circuitry that facilitates host-microbe symbiosis.
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