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Together, our findings suggest that IL-24 may function not only as a biomarker of type 2 inflammation but also as an upstream regulator of IL-13driven airway pathology, particularly in early-onset asthma

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falciparum contributing to the oxidative stress response, an aspect that has been previously associated with artemisinin resistance (Siddiqui et al., 2017) but not associated with any molecule transported from the mitochondria