Instructions: In this task, you are given an abstract of article. Your task is to generate title for this article. Preferred titles are under thirty words.
Input: 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 (IL-1) directly activated human ILC2s and that IL-12 induced the conversion of these activated ILC2s into interferon- (IFN-)-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.
Output:
IL-1, IL-4 and IL-12 control the fate of group 2 innate lymphoid cells in human airway inflammation in the lungs