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IL-4 and IL-13 traffic EOS directly to airway tissues, leading to asthma symptoms and increasing the risk of exacerbations and lung function decline.

IL-5 promotes the trafficking, differentiation, release, and survival of EOS.

Th2 cell differentiation1,2 

Asthma triggers can activate the alarmin pathway while concurrently activating dendritic cells directly, which differentiate Th0 cells into Th2 cells and, along with ILC2 cells, produce IL-4, IL-13, and IL-5.

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