Group 2 innate lymphoid cells are the earliest recruiters of eosinophils in lungs of patients with allergic asthma

Protection against helminths as well as immune response to allergens in atopic subjects, consists not only of adaptive responses orchestrated by type 2 T helper (Th2) cells, but also involves the activation of a recently discovered subset of innate immunity cells. These cells, the group 2 innate lymphoid cells (ILC2), have been recently characterized in both mice and humans, and represent a cell subset of the innate immunity specialized in the induction an maintenance of type 2 inflammation. Because of their similarities in the function and requirement of transcriptional machinery, it it is considered that both Th2 cells and ILC2 collaborate during type 2 immune responses, including protection against parasites and the genesis of allergic inflammation. ILC2 preferentially localize to the interface between the host and the environment (lung, intestine, skin), and this strategical localization allow them to represent a critical link between the innate and adaptive components of type 2 immunity. ILC2 differ from Th2 cells mainly because of the lack of T-cell receptor (TCR), but they can be activated by several factors, including cystenil-leucotriens, PGD2, IL-2, IL-4, IL-7, IL-15, and some toll-like receptor ligands. Beyond these factors, the epithelial derived cytokines IL-25, IL-33, and TSLP represent the major source of their activation. Once activated, ILC2 are capable of producing IL-4, IL-13 and large amounts of IL-5, whose production is considered to be an hallmark of their function. Indeed, ILC2s have been shown to accumulate at the site of eosinophilic inflammation, including nasal polyps and sinus mucosa in subjects with chronic rhinosinusitis, skin lesions in atopic dermatitis, and of course in lungs of patients with bronchial asthma.