Asthma is a chronic pulmonary disease, highly associated with immune disorders. The typical symptoms of asthma include airway hyperresponsiveness (AHR), airway remodeling, mucus overproduction, and airflow limitation. The etiology of asthma is multifactorial and affected by genetic and environmental factors. Increasing trends toward dysbiosis, smoking, stress, air pollution, and a western lifestyle may account for the increasing incidence of asthma. Based on the presence or absence of eosinophilic inflammation, asthma is mainly divided into T helper 2 (Th2) and non-Th2 asthma. Th2 asthma is mediated by allergen-specific Th2 cells, and eosinophils activated by Th2 cells via the secretion of interleukin (IL)-4, IL-5, and IL-13. Different from Th2 asthma, non-Th2 asthma shows little eosinophilic inflammation, resists to corticosteroid treatment, and occurs mainly in severe asthmatic patients. Previous studies of asthma primarily focused on the function of Th2 cells, but, with the discovery of non-Th2 asthma and the involvement of innate lymphoid cells (ILCs) in the pathogenesis of asthma, tissue-resident innate immune cells in the lung have become the focus of attention in asthma research. Currently, innate-like lymphocytes (ILLs) and ILCs as important components of the innate immune system in mucosal tissues are reportedly involved in the pathogenesis of or protection against both Th2 and non-Th2 asthma. These findings of the functions of different subsets of ILLs and ILCs may provide clues for the treatment of asthma.
Keywords: Innate lymphoid cells (ILCs); Innate-like lymphocytes (ILLs); Non-Th2 asthma; Pathogenesis; Protection; Th2 asthma.