先天性淋巴细胞
免疫学
炎症
白细胞介素33
白细胞介素22
生物
细胞因子
白细胞介素
RAR相关孤儿受体γ
白细胞介素17
肺
医学
促炎细胞因子
先天免疫系统
白细胞介素23
白细胞介素8
细胞生物学
免疫系统
白细胞介素13
支气管肺泡灌洗
作者
Suzanne M. Bal,Jochem H. Bernink,Maho Nagasawa,Jelle Groot,Medya Shikhagaie,Kornel Golebski,Cornelis M. van Drunen,René Lutter,René E. Jonkers,Pleun Hombrink,Mélanie Bruchard,Julien Villaudy,J. Marius Munneke,Wytske J. Fokkens,Jonas Erjefält,Hergen Spits,Xavier Romero Ros
摘要
Group 2 innate lymphoid cells (ILC2s) secrete type 2 cytokines, which protect against parasites but can also contribute to a variety of inflammatory airway diseases. We report here that interleukin 1β (IL-1β) directly activated human ILC2s and that IL-12 induced the conversion of these activated ILC2s into interferon-γ (IFN-γ)-producing ILC1s, which was reversed by IL-4. The plasticity of ILCs was manifested in diseased tissues of patients with severe chronic obstructive pulmonary disease (COPD) or chronic rhinosinusitis with nasal polyps (CRSwNP), which displayed IL-12 or IL-4 signatures and the accumulation of ILC1s or ILC2s, respectively. Eosinophils were a major cellular source of IL-4, which revealed cross-talk between IL-5-producing ILC2s and IL-4-producing eosinophils. We propose that IL-12 and IL-4 govern ILC2 functional identity and that their imbalance results in the perpetuation of type 1 or type 2 inflammation.
科研通智能强力驱动
Strongly Powered by AbleSci AI