[The immunopathology of asthma].

Type 2 (T2) high asthma, characterized by T2 markers such as eosinophilia, is driven by type 2 innate lymphoid cells (ILC2) and allergen-activated T helper (Th2) cells. Epithelial-derived cytokines called alarmins, IL-33, TSLP, IL-25 and TL1A, acting on dendritic cells and ILC2, are key in driving both allergic and non-allergic T2 high asthma. Alarmins are produced in response to allergens, pathogens, pollutants etc. Cytokines produced by Th2 cells and ILC2 cause the immunopathology of asthma including eosinophilia, mast cell activation, goblet cell hyperplasia and fibrosis, which in turn causes airway hyperresponsiveness, bronchoconstriction, tissue remodeling and mucus hypersecretion. However, asthma also occurs in patients devoid of T2 markers. The immunological mechanisms of so called T2 low asthma seems to be related to IL-22/IL-17 cytokines and/or inflammasome activation, but much research remains to unravel the etiology and mechanisms to identify ways of effectively treating T2 low asthma.