IL-1β, IL-4 and IL-12 control the fate of group 2 innate lymphoid cells in human airway inflammation in the lungs

Suzanne M. Bal; Jochem H. Bernink; Maho Nagasawa; Jelle Groot; Medya M. Shikhagaie; Kornel Golebski; Cornelis M. van Drunen; Rene Lutter; Rene E. Jonkers; Pleun Hombrink; Melanie Bruchard; Julien Villaudy; J. Marius Munneke; Wytske Fokkens; Jonas S. Erjefält; Hergen Spits; Xavier Romero Ros

doi:https://doi.org/10.1038/ni.3444

IL-1β, IL-4 and IL-12 control the fate of group 2 innate lymphoid cells in human airway inflammation in the lungs

Suzanne M. Bal, Jochem H. Bernink, Maho Nagasawa, Jelle Groot, Medya M. Shikhagaie, Kornel Golebski, Cornelis M. van Drunen, Rene Lutter, Rene E. Jonkers, Pleun Hombrink, Melanie Bruchard, Julien Villaudy, J. Marius Munneke, Wytske Fokkens, Jonas S. Erjefält, Hergen Spits, Xavier Romero Ros

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Abstract

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

Original language	English
Pages (from-to)	636-645
Journal	Nature immunology
Volume	17
Issue number	6
DOIs	https://doi.org/10.1038/ni.3444
Publication status	Published - 2016

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https://doi.org/10.1038/ni.3444

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Bal, S. M., Bernink, J. H., Nagasawa, M., Groot, J., Shikhagaie, M. M., Golebski, K., van Drunen, C. M., Lutter, R., Jonkers, R. E., Hombrink, P., Bruchard, M., Villaudy, J., Munneke, J. M., Fokkens, W., Erjefält, J. S., Spits, H., & Ros, X. R. (2016). IL-1β, IL-4 and IL-12 control the fate of group 2 innate lymphoid cells in human airway inflammation in the lungs. Nature immunology, 17(6), 636-645. https://doi.org/10.1038/ni.3444

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title = "IL-1β, IL-4 and IL-12 control the fate of group 2 innate lymphoid cells in human airway inflammation in the lungs",

abstract = "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",

author = "Bal, {Suzanne M.} and Bernink, {Jochem H.} and Maho Nagasawa and Jelle Groot and Shikhagaie, {Medya M.} and Kornel Golebski and {van Drunen}, {Cornelis M.} and Rene Lutter and Jonkers, {Rene E.} and Pleun Hombrink and Melanie Bruchard and Julien Villaudy and Munneke, {J. Marius} and Wytske Fokkens and Erjef{\"a}lt, {Jonas S.} and Hergen Spits and Ros, {Xavier Romero}",

year = "2016",

doi = "https://doi.org/10.1038/ni.3444",

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journal = "Nature immunology",

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Bal, SM, Bernink, JH, Nagasawa, M, Groot, J, Shikhagaie, MM, Golebski, K , van Drunen, CM , Lutter, R , Jonkers, RE, Hombrink, P, Bruchard, M, Villaudy, J, Munneke, JM, Fokkens, W, Erjefält, JS, Spits, H & Ros, XR 2016, 'IL-1β, IL-4 and IL-12 control the fate of group 2 innate lymphoid cells in human airway inflammation in the lungs', Nature immunology, vol. 17, no. 6, pp. 636-645. https://doi.org/10.1038/ni.3444

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T1 - IL-1β, IL-4 and IL-12 control the fate of group 2 innate lymphoid cells in human airway inflammation in the lungs

AU - Bal, Suzanne M.

AU - Bernink, Jochem H.

AU - Nagasawa, Maho

AU - Groot, Jelle

AU - Shikhagaie, Medya M.

AU - Golebski, Kornel

AU - van Drunen, Cornelis M.

AU - Lutter, Rene

AU - Jonkers, Rene E.

AU - Hombrink, Pleun

AU - Bruchard, Melanie

AU - Villaudy, Julien

AU - Munneke, J. Marius

AU - Fokkens, Wytske

AU - Erjefält, Jonas S.

AU - Spits, Hergen

AU - Ros, Xavier Romero

PY - 2016

Y1 - 2016

N2 - 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

AB - 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

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DO - https://doi.org/10.1038/ni.3444

M3 - Article

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JO - Nature immunology

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