先天性淋巴细胞
RAR相关孤儿受体γ
C-C趋化因子受体6型
下调和上调
孤儿受体
生物
细胞因子
免疫学
白细胞介素22
白细胞介素
细胞生物学
免疫系统
炎症
医学
转录因子
免疫
趋化因子
趋化因子受体
遗传学
FOXP3型
基因
作者
Jochem H. Bernink,Yoichiro Ohne,Marcel B. M. Teunissen,Jingya Wang,Jincheng Wu,Lisette Krabbendam,Christine Guntermann,Richard Volckmann,Jan Koster,Sophie van Tol,Iván Hernández Ramírez,Yashaswi Shrestha,Menno A. de Rie,Hergen Spits,Xavier Romero Ros,Alison Humbles
标识
DOI:10.1038/s41590-019-0423-0
摘要
Here we identify a group 2 innate lymphoid cell (ILC2) subpopulation that can convert into interleukin-17 (IL-17)-producing NKp44- ILC3-like cells. c-Kit and CCR6 define this ILC2 subpopulation that exhibits ILC3 features, including RORγt, enabling the conversion into IL-17-producing cells in response to IL-1β and IL-23. We also report a role for transforming growth factor-β in promoting the conversion of c-Kit- ILC2s into RORγt-expressing cells by inducing the upregulation of IL23R, CCR6 and KIT messenger RNA in these cells. This switch was dependent on RORγt and the downregulation of GATA-3. IL-4 was able to reverse this event, supporting a role for this cytokine in maintaining ILC2 identity. Notably, this plasticity has physiological relevance because a subset of RORγt+ ILC2s express the skin-homing receptor CCR10, and the frequencies of IL-17-producing ILC3s are increased at the expense of ILC2s within the lesional skin of patients with psoriasis.
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