期刊
NATURE IMMUNOLOGY
卷 17, 期 6, 页码 636-+出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.3444
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- European Research Council (Advanced ERC grant-AsthmaVir) [341038]
- European Research Council (ERC) [341038] Funding Source: European Research Council (ERC)
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 1 beta (IL-1 beta) directly activated human ILC2s and that IL-12 induced the conversion of these activated ILC2s into interferon-gamma (IFN-gamma )-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.
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