Asthma is one of the most prevalent chronic diseases worldwide, affecting approximately 10% of adults and an even greater proportion of children. Type-2 innate lymphoid cell (ILC2)- and type 2 helper T cell (TH2)-driven type 2 inflammation is a critical contributor to the pathogenesis of this disease. Various triggers, such as protease allergens, helminth parasites, fungi and influenza virus, can stimulate epithelial cells to release alarmins such as IL-33, IL-25 and thymic stromal lymphopoietin (TSLP) to drive ILC2s and TH2 activation. In this review, we provide some latest advances in our understanding of the role of ILC2s and TH2 in asthma. With regard to TH2, we focus on transcriptional factors, ubiquitination, Notch signaling pathway and clinical research. In the case of ILC2s, we concentrate on transcriptional factors, co-stimulatory molecules, epigenetic and metabolic pathways in a cell-intrinsic way and on cell-cell interaction in a cell-extrinsic way. The questions in this field are also addressed.
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