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. 2021 Sep 22;12:733324. doi: 10.3389/fimmu.2021.733324

Figure 2.

Figure 2

ILC involvement in asthma. Upon allergen detection by airway epithelium, 1) ILC2s are activated by signals released by the airway epithelial cells and other activated immune cells, producing type 2 cytokines such as IL-4, IL-5, and IL-13 in allergic asthma. 2) IL-5 is key for eosinophil recruitment and activation in the lung (77) and 3) IL-13 mediates dendritic cell migration to the lymph nodes, promoting T cell differentiation into effector Th2 cells, which mediate B cell class-switching and IgE production (78). 4) ILC2-derived IL-13 also acts on the airway epithelium to induce airway hyperresponsiveness, mucus overproduction and disruption of barrier integrity (43, 79, 80). 5) ILC2-derived IL-4 may potentially inhibit Treg production in asthma (81). 6) NK cells play an ambiguous role in asthma with both disease-driving and disease-modulatory activity shown. 7) ILC3s/LTi cells and possibly ILC1s contribute to obesity-related asthma and potentially non-allergic, severe asthma or ACO through production of IL-17 (82). 8) ILCregs may regulate asthma by inhibiting eosinophil recruitment through IL-10 (83).