The Functional Role of Group 2 Innate Lymphoid Cells in Asthma

Asthma is a heterogeneous disease characterized by chronic airway inflammation. Group 2 innate lymphoid cells (ILC2) play an important role in the pathogenesis of asthma. ILC2s lack antigen-specific receptors and respond to epithelial-derived cytokines, leading to the induction of airway eosinophilic inflammation in an antigen-independent manner. Additionally, ILC2s might be involved in the mechanism of steroid resistance. Numerous studies in both mice and humans have shown that ILC2s induce airway inflammation through inflammatory signals, including cytokines and other mediators derived from immune or non-immune cells. ILC2s and T helper type 2 (Th2) cells collaborate through direct and indirect interactions to organize type 2 immune responses. Interestingly, the frequencies or numbers of ILC2 are increased in the blood and bronchoalveolar lavage fluid of asthma patients, and the numbers of ILC2s in the blood and sputum of severe asthmatics are significantly larger than those of mild asthmatics. These findings may contribute to the regulation of the immune response in asthma. This review article highlights our current understanding of the functional role of ILC2s in asthma.

Automated summary

Asthma is characterized by chronic airway inflammation. Group 2 innate lymphoid cells (ILC2) play a crucial role in its pathogenesis and are involved in both steroid resistance and the induction of airway eosinophilic inflammation. Studies have shown that ILC2s induce airway inflammation through interactions with cytokines and other mediators from immune and non-immune cells, collaborating with T helper type 2 cells to organize type 2 immune responses. The increased frequencies of ILC2s in the blood and bronchoalveolar lavage fluid of asthma patients, especially in severe asthmatics, contribute to the regulation of immune response in asthma.