The current review explains the function of several kinds of innate lymphoid cells (ILCs) in the development of asthma inflammatory phenotypes by comparing results from murine asthma models to human research. Patients with steroid-insensitive asthma require novel therapy alternatives. This study discusses developing strategies for targeting ILCs or their upstream or downstream molecules. ILCs, particularly type 2 ILCs (ILC2s), are activated by alarmins such as IL-33 following allergen triggering of the airway epithelium in eosinophilic asthma. This causes ILC2 to produce IL-5 and IL-13, resulting in eosinophilic inflammation and airway hyperreactivity. Type 3 ILCs (ILC3s) have been linked to obesity-induced asthma via IL-1 production by macrophages, which leads to the formation of ILC3s and the release of IL-17. ILC1s may have a role in severe asthma, although their involvement is currently understudied.
Several investigations have shown that ILC2s have a role in the development of eosinophilic inflammation in allergic and nonallergic asthmatic patients, primarily through the action of IL-5, IL-13, IL-33, and thymic stromal lymphopoietin. The role of ILC3s and ILC1s in asthmatic patients is little understood. More research is needed to substantiate the notion that these additional kinds of ILCs have a role in asthma aetiology, most likely in nonallergic asthma phenotypes.