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

Suzanne M Bal, et al.

Nat Immunol. 2016 Jun;17(6):636-45.

Speaker: Wen-Chien Chen(陳玟蒨)             Time: 13:10~14:00, Dec. 13, 2017

Commentator: Dr. Chi-Chang Shieh(謝奇璋 醫師)         Place: Room 601

Abstract:

   Group 2 innate lymphoid cells(ILC2s) play the crucial role of secreting type 2 cytokines in response to helminth infection, and have also been implicated in the development of inflammatory airway diseases. Chronic obstructive pulmonary disease (COPD) is a heterogeneous airway disease with elements of type 1 inflammation, including elevated production of IL-12, IL-18 and IFN-γ, and accumulation of ILC1s. Chronic rhinosinusitis with nasal polyps (CRSwNP) is type 2 inflammatory diseases and produces Th2-associated cytokines(IL-4, IL-5, and IL-13). In CRSwNP, ILC2 is the majority subset of ILC. This group reports that interleukin 12(IL-12) governs the transdifferentiation of ILC2s into IFN-γ-producing ILC1s while stimulating with IL-1β in inflamed tissue in COPD. In contrast, IL-4 promotes ILC2 maintenance and proliferation, and restores the functional identity of ILC2s in CRSwNP. Besides, it reveals cross-talk between IL-5-producing ILC2s and IL-4-producing eosinophils in CRSwNP. The alteration of ILC population and ILC2 functional identity are dominated by IL-12 and IL-4, which may result in type 1 or type 2 inflammation when IL-12 and IL-4 are imbalanced.

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