IL-1β, IL-4 and IL-12 control the fate of group 2 innate lymphoid cells in human airway inflammation in the lungs.
Fiche publication
Date publication
juin 2016
Journal
Nature immunology
Auteurs
Membres identifiés du Cancéropôle Est :
Dr BRUCHARD Mélanie
Tous les auteurs :
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
Lien Pubmed
Résumé
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.
Mots clés
Animals, Cell Differentiation, Cell Plasticity, Cells, Cultured, Eosinophils, immunology, Female, Humans, Immunity, Innate, Interferon-gamma, metabolism, Interleukin-12, metabolism, Interleukin-1beta, metabolism, Interleukin-4, metabolism, Lymphocyte Activation, Lymphocytes, immunology, Mice, Mice, SCID, Nasal Polyps, immunology, Pneumonia, immunology, Pulmonary Disease, Chronic Obstructive, immunology, Rhinitis, immunology, Sinusitis, immunology, Th1 Cells, immunology, Th1-Th2 Balance, Th2 Cells, immunology
Référence
Nat. Immunol.. 2016 06;17(6):636-45