Over the past two decades, innate lymphoid cells (ILCs) have emerged as critical early responders in immune responses, orchestrating inflammation through cytokine production independent of antigen specificity. Early after their discovery, Group 2 ILCs (ILC2s) were found to produce high levels of IL-5 and IL-13 upon stimulation by epithelial-derived alarmins IL-33, IL-25, and thymic stromal lymphopoietin (TSLP). Since then, a robust amount of literature has emerged that places ILC2s as central to type 2 inflammatory diseases, including rhinosinusitis and asthma. Recent work continues to rapidly expand our knowledge of how ILC2s are modulated and contribute to immune disease and maintain homeostasis. This review will focus on recent updates to our understanding of ILC2s in the context of neural and endocrine modulation, memory/trained immunity, cellular fate/plasticity, and adaptive type 2 responses.
Taylor A. Doherty (2026) studied this question.