IL-1ß, IL-4 and IL-12 control the fate of group 2 innate lymphoid cells in human airway inflammation in the lungs.
Nat Immunol
; 17(6): 636-45, 2016 06.
Article
de En
| MEDLINE
| ID: mdl-27111145
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 1ß (IL-1ß) 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.
Texte intégral:
1
Collection:
01-internacional
Base de données:
MEDLINE
Sujet principal:
Pneumopathie infectieuse
/
Sinusite
/
Lymphocytes
/
Rhinite
/
Polypes du nez
/
Interleukine-4
/
Interleukine-12
/
Broncho-pneumopathie chronique obstructive
/
Granulocytes éosinophiles
/
Interleukine-1 bêta
Limites:
Animals
/
Female
/
Humans
Langue:
En
Journal:
Nat Immunol
Sujet du journal:
ALERGIA E IMUNOLOGIA
Année:
2016
Type de document:
Article
Pays d'affiliation:
Pays-Bas